emDOCs â Emergency Medicine Education

EM Mindset: Imposter Syndrome

Wed, 30 Sep 2020 14:46:44 GMT

Author: Cassandra Newburg, MD (@CasscIn, EM Attending Physician, University of Massachusetts Emergency Medicine) // Reviewed by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

First shift as an attending, your badge doesn’t work, you don’t know the number to call to let you in, in fact you don’t know any numbers yet and try knocking on the large windowless wooden door. As if you weren’t feeling enough like an imposter already, just yesterday you were a PGY-3 and now you are suddenly an attending physician. Am I ready for this?

One kind soul opens the door, you adjust your white coat and you start your shift. You are plugging along, figuring out flow at the new hospital, seeing patients and then all of a sudden you get called emergently into a room.

Case 1:

Patient presents with dizziness and generalized fatigue for a week. Daughter at bedside listing out medications. Monitor reads ventricular tachycardia. BP is normal. Patient is at her baseline mental status. Stabilized patient, unable to figure out diagnosis, enlisted help. Cardiology joins me at bedside. Cardiology figures out patient is on digoxin. Symptoms consistent with chronic dig toxicity although normal level. Cardiology also sees an EKG from clinic which shows slow onset atrial fibrillation. Cardiology recommends giving a vial of DigiFab, admitted to cardiology intensive care unit.

Lesson Learned: Chronic Dig Toxicity

Chronic dig toxicity has higher mortality (15-30%)
Vague symptoms (weak, dizzy, tired)
Dig levels: false positives and negatives based on timing of testing and chronic dig toxicity can have therapeutic range levels
Treatment: DigiFab/Digibind is definitive treatment

New attending advice: Ask for help when you need it. Be humble and realize you might not get everything or know everything – especially things you did not come across in residency. In addition, utilize your support system when you feel like you didn’t do the best you could.

Case 2:

One of the wonderful shifts working with a second year resident. We see a patient who presents with lower back pain, fever, and urinary urgency. Recently started on a new medication for diabetes, dapagliflozin. Noted his blood sugar levels at home have been normal since starting the new medication. Patient does not know when his fever started. Urinalysis shows glucose and ketones, no sign of infection in the urinalysis. Complete blood count shows lymphopenia with a low absolute lymphocyte count. Complete metabolic panel shows an elevated anion gap, decreased bicarbonate level, normal glucose, normal kidney function. Imaging studies unremarkable. Elevated serum ketones. + COVID. Patient found to have COVID induced euglycemic DKA.

Lesson learned: Euglycemic DKA

Can be caused by SGLT-2 inhibitors, exact mechanism unknown
Presents with normal glucose but elevated serum ketones and elevated anion gap
Treatment similar to DKA with insulin utilized to close anion gap however will also require addition of glucose to prevent hypoglycemia

New attending advice: We don’t know everything; there is always more to learn. Keep using the resources you used in residency and talk to your colleagues and/or mentors. Also a reminder to review all of your results and make sure you can explain the tests you order and the findings. The resident and I worked through this case together to figure out what was happening.

Case 3:

Final case of first year as an attending: Called out of a patient’s room to an unresponsive patient. No pulses noted, so we initiated CPR. Tech who pulled patient from car tells us that family member is on their way. I look and see a very ill appearing patient, cachectic and frail, advanced in years. One member of the team asks if I am going to get a definitive airway. Patient bagging easily, I made the decision to defer. We continue basic CPR until patient’s spouse comes in to the emergency department. I sit down and talk to the patient’s spouse. We discuss patient’s presentation and how they have been doing over the past year. We also discuss what the patient wishes and what the family wishes. I take my time, find out that the patient did not wish to be intubated or have compressions performed or given resuscitation medications. Resuscitation efforts are stopped, patient’s spouse is able to have time to say goodbye to the patient.

Lesson learned: Sometimes the right thing to do is to do nothing.

New attending advice: Stand there, don’t just do something. Get comfortable with end of life care discussions. Try to talk to family as soon as possible to find out patient wishes. You know medicine, resuscitations, and procedures but make sure you are acting in accordance with patient and family wishes.

EM is humbling in so many ways; asking for help is not a sign of failure, and imposter syndrome is a real thing. Listen to your patients and families and think about the results you have and the presentation in front of you. Final shift as a first year attending draws to an end and I walk out the large wooden intimidating doors with a sigh of relief. I look forward to the years ahead practicing in this amazing specialty.

Sources:

https://litfl.com/digoxin-toxicity-ccc/

https://emergencymedicinecases.com/low-slow-poisoning/

https://www.uptodate.com/contents/sodium-glucose-co-transporter-2-inhibitors-for-the-treatment-of-hyperglycemia-in-type-2-diabetes-mellitus

https://www.aliem.com/euglycemic-dka/

https://rebelem.com/euglycemic-dka-not-myth/

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Medical Malpractice Insights: Do not mistake this for simple vertigo

Tue, 29 Sep 2020 07:55:30 GMT

Here’s another case from Medical Malpractice Insights – Learning from Lawsuits, a monthly email newsletter for ED physicians. The goal of MMI-LFL is to improve patient safety, educate physicians and reduce the cost and stress of medical malpractice lawsuits. To opt in to the free subscriber list, click here.

Conference Alert: I highly recommend the annual October “Diagnostic Error in Medicine” conference of the Society to Improve Diagnosis in Medicine. It’s virtual this year – and affordable. https://www.improvediagnosis.org/2020conference/

Chuck Pilcher, MD, FACEP

Editor, Med Mal Insights

Posterior Circulation Stroke

Do not mistake this for simple vertigo

Facts: A 54-year-old male experiences sudden onset of neck pain, nausea, and diaphoresis while driving to work. He pulls to the side of the freeway and calls 911. En route to Hospital A he becomes dizzy and on arrival to the ED is noted to be diaphoretic, clammy, bradycardic, and “appearing uncomfortable.” His neck pain worsens with motion and radiates to his head. A remote history of labyrinthitis is elicited by the emergency physician (who is at the tail end of a night shift). He is given metoclopramide and diphenhydramine and discharged with a diagnosis of cervical strain and positional vertigo. Two hours later he is worse and calls 911 again. This time he is taken to Hospital B where he is noted to be hemiparetic. A non-contrast head CT is non-diagnostic. A CTA is recommended but not done for 5 hours. It shows a vertebral artery dissection (VAD.) He is transferred to Hospital C for care of his stroke.

Plaintiff: Hospital A: I had a classic presentation of a VAD. You never asked me how my symptoms were different than my labyrinthitis years ago. You should have done an MRA and found it on my first visit, especially since your hospital is a stroke center. Hospital B: You should have gotten a CTA or MRA immediately for my classic symptoms; the non-contrast CT was unnecessary and delayed my care. With earlier care I would not be disabled now.

Defense: Your symptoms were consistent with labyrinthitis and a neck strain. Your CT at Hospital B was normal, as it would have been at Hospital A. There’s no clear treatment for a VAD, so it doesn’t make any difference.

Result: Confidential settlement against Hospital A, the emergency physician, and Hospital B for undisclosed amount after 3 years of litigation and an estimated $100,000 in legal costs.

Takeaways:

Sudden onset of “cervical strain” and “positional vertigo” while driving to work? To the point of calling 911 and leaving your car on the side of the road? What were you thinking?
Sudden onset of neck pain, dizziness, sweating, head pain, and nausea equals a classic presentation of a vertebral artery dissection (VAD) or cervical/carotid artery dissection (CAD).
Not all VADs or CADs are classic;
42% of patients with VAD do not have vertigo.
49% do not have headache.
54% do not have neck pain.
Sweating is always a bad sign.
Perform a thorough neurologic exam and evaluate for signs of central vertigo/cerebellar pathology.
- Evaluate cranial nerves, gait, truncal ataxia, finger to nose/heel to shin, rapid alternating movements, test of skew, motor, and sensation.

References/Further Resources:

Clinical Characteristics of Symptomatic Vertebral Artery Dissection: A Systematic Review. Gottesman RF et al. Neurologist. 2012;18(5):245-254. Great review and summary in Medscape -> medscape.com/viewarticle/771223_1
http://www.emdocs.net/cervical-artery-dissection-the-elusive-diagnosis/
http://www.emdocs.net/posterior-circulation-strokes-why-do-we-miss-them-and-how-do-we-improve/
http://www.emdocs.net/posterior-circulation-strokes-dizziness-pearls-pitfalls/

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Emphysematous Pyelonephritis: ED Presentation, Evaluation, and Management

Mon, 28 Sep 2020 07:27:13 GMT

Author: Frances Rusnack, DO, MS (EM Resident Physician, Mount Sinai Morningside/West) // Reviewed by: Summer Chavez, DO, MPH, MPM (Health Policy Fellow, Georgetown University/Medstar); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case

A 64-year-old female with a past medical history of type 2 insulin-dependent diabetes presents to the emergency department with altered mental status. She was brought in by her spouse who reports 5 days of dysuria with worsening left-sided abdominal and flank pain, nausea, and vomiting. She has no history of abdominal surgeries or kidney stones and he denies possible trauma or accidental overdose.

Vitals: BP 102/74, HR 109, RR 16, T 39°C, SpO2 99% RA. The patient is oriented to person only with a normal neurological exam and no signs of external trauma. Lungs are clear to auscultation bilaterally, no murmurs are appreciated, and she has no visible rash. She has significant left mid abdominal and left costovertebral angle tenderness. Urinalysis is positive for leukocyte esterase, nitrites, many WBC, and large bacteria. She is found to have a lactate of 4.2 mmol/L, leukocytosis of 23 x10⁹ per L, thrombocytopenia of 50 x10⁹ per L, and an elevated creatinine to 2.9 mg/dL. CT abdomen/pelvis with IV contrast demonstrates gas in the left renal parenchyma extending to the perinephric space.

What are the next steps in management?

Background

Emphysematous pyelonephritis (EPN) is a relatively uncommon spectrum of disease characterized by gas forming bacteria causing a severe necrotizing infection of the renal parenchyma and surrounding areas.^1,2 Gas production can be local or diffuse and may spread to the perinephric spaces.^1,3

Epidemiology & Pathophysiology

EPN is a rare diagnosis. A comprehensive meta-analysis from 2013 identified a total of 628 patients.⁴ EPN often occurs in diabetic patients with an average age of 60-years old.^1,3 Females are disproportionately affected at a ratio of 3:1 which is thought to be related to increased incidence of bacteriuria.^1,4-6

The most common risk factor for the development of EPN is diabetes mellitus, type 1 and type 2.^1,4-6 Up to 90% of EPN patients have either type 1 or type 2 diabetes mellitus.³ The assumption is that elevated blood glucose levels create a favorable environment for gas forming bacteria in tissues with microvascular disease and poor perfusion.^3-5,9 Gas-forming bacteria use the glucose for fermentation, producing hydrogen peroxide and carbon dioxide gases.^3,4 Other risk factors include immunocompromised state and history of renal transplant or polycystic kidney disease. Urinary tract obstruction has been observed in up to 34% of EPN cases.⁴

The most commonly identified bacteria are enteric gram-negative facultative anaerobes such as Escherichia coli (69%) and Klebsiella pneumoniae (29%).^1,3 Other organisms found include Acinetobacter, Proteus, Streptococcus, andPseudomonas species.^5-7 Anaerobes (Bacteroides, Clostridium) and fungi (Candida, Aspergillus fumigatus) have also been associated.^1,6-8Bacteremia occurs in up to 50% of cases and the same organisms are found in urine/pus cultures.³

Prognosis

Mortality rates from published studies range from 11% to 42% with an average of about 25%.^3,4,14,19 Without treatment, EPN is fatal. Some factors associated with a worse prognosis include delayed diagnosis, multiple comorbidities, bilateral EPN (Class 4), Type I EPN (mortality 69%), polymicrobial infection, conservative management only, shock, altered mental status, creatinine >2.5 mg/dl, thrombocytopenia, hypoalbuminemia, and a decreased leukocyte to platelet ratio.^{1,2,4,7,9,18,19} A 2007 meta-analysis did not find an association between overall mortality and diabetes, female sex, age >50, or nephrolithiasis.¹⁹

Clinical Presentation of EPN

Patients usually present with vague complaints or symptoms typical of acute pyelonephritis such as pyuria (78%), fever (75%), abdominal or flank pain (70%), nausea, and vomiting.^1,5,6,9,19 To review the evaluation and management of pyelonephritis, please visit emDOCs: Pyelonephritis: It’s not always so straightforward… Less common signs and symptoms include dyspnea, dysuria, pneumaturia, or crepitus.¹The most common physical exam finding is costovertebral angle tenderness.^1,6Because of this overlap in clinical presentation, patients may initially be treated for presumed acute pyelonephritis. An inadequate response to typical treatment may then prompt further imaging and subsequent EPN diagnosis.¹⁰ Some patients may be very ill on initial presentation with acute renal failure, dyspnea, altered mental status or other signs of septic shock.^1,5,6,9 A high index of suspicion is therefore needed in patients with EPN risk factors such as diabetes.

Differential Diagnosis

While an uncommon diagnosis, EPN should be considered in patients who are severely ill with septic shock or who have significant risk factors such as DM, female sex, or urinary obstruction and do not respond to usual treatment for pyelonephritis. The differential diagnosis for EPN includes:

Acute pyelonephritis

Nephrolithiasis

Iatrogenic instrumentation of GU system

Xanthogranulomatous pyelonephritis

Infected nephrolithiasis

Renal abscess

Perinephric abscess

Pelvic inflammatory disease

Prostatitis

Epididymitis

Diverticulitis

Evaluation

Laboratory Studies

Findings consistent with EPN include pyuria, elevated creatinine, thrombocytopenia (46% of patients), and bacteremia.^1,3,4 Initial workup should include CBC, BMP, urinalysis, urine culture, and blood cultures.¹

Imaging Studies

CT Imaging:

While acute pyelonephritis is a clinical diagnosis, imaging should be considered in patients who appear toxic, have comorbidities, or do not respond to usual treatment.¹⁰ The diagnosis of EPN requires radiographic evidence of gas in the renal parenchyma and surrounding areas.^2,4,11The best imaging modality is CT scan of the abdomen and pelvis with 100% detection rate.^9,4 Contrast-enhanced CT, unless contraindicated, is preferred because it allows for better visualization of the gas for staging and shows the extent of renal destruction.^1,4,11 CT will also readily detect calculi and can be used for follow up imaging to guide continued management.^1,2

CT abdomen/pelvis shows enlargement of the right kidney, heterogenous contrast enhancement and multiple parenchymal collections with gas locules. Case courtesy of <a href=”https://radiopaedia.org/”>Radiopaedia.org</a>. From the case <a href=”https://radiopaedia.org/cases/11386″>rID: 11386</a>

Abdominal X-Ray:

KUB can be useful in detecting EPN, more so in later stages of disease.¹ KUB may show air within the renal system, destruction of the renal parenchyma, loss of the psoas muscle outline, or sometimes calculi.¹ However, KUB is only accurate in 53.2% to 65% of cases.^4,14

Abdominal x-ray shows an enlarged right kidney overlying gas extending to the perinephric space. There are also paraspinal linear gas shadows indicating retroperitoneal air. Case courtesy of Dr. Mohammad Taghi Niknejad, <ahref=”https://radiopaedia.org/”>Radiopaedia.org</a>. From the case <ahref=”https://radiopaedia.org/cases/21473”>rID: 21473</a>

Ultrasound:

Ultrasound is a fast, inexpensive, and radiation-free imaging modality that can provide quick evidence towards the diagnosis of EPN.¹² Ultrasound may show intrarenal, intraurethral, or intracystic air artifacts seen as dirty shadowing (shadowing with irregular borders due to reflections at the gas-tissue interface) and a-lines (reverberation artifacts).^11-13Studies on POCUS in EPN are limited and it is only accurate in 69% of cases.^13,14 Additionally, POCUS is provider dependent and hindered by body habitus and nearby bowel gas.¹⁴ A follow up CT should be used to confirm and classify EPN.¹⁴

Ultrasound shows left kidney enlargement, poor corticomedullary differentiation, and linear air shadows. Case courtesy of Dr. Maulik S Patel, <a href=”https://radiopaedia.org/”>Radiopaedia.org</a>. From the case <a href=”https://radiopaedia.org/cases/17283″>rID: 17283</a>

Classification

There are two main classification systems for EPN. In 1996, Wan et al. described two types of EPN.¹⁵ In 2000, Huang and Tseng developed a more detailed classification system that coincides with treatment and is more commonly used.³

Wan et al. Classification System¹⁵

Type I: Renal parenchymal destruction with absence of fluid or presence of streaky/mottled gas

Type II: Renal or perirenal fluid with bubbly/loculated gas or presence of gas in the collecting system

Huang and Tseng Classification System³

Class 1: Gas in collecting system only

Class 2: Gas in the renal parenchyma

Class 3A: Gas or abscess extension to the perinephric space

Class 3B: Gas or abscess extension to the pararenal space beyond Gerota’s fascia

Class 4: Bilateral EPN or EPN in a solitary kidney

Treatment

All patients should undergo general resuscitative measures with a focus on hemodynamics, glucose control, and early antibiotics.^1,14,16 Antibiotic choice should be based on local resistance patterns to cover gram-negative bacteria such as fourth-generation cephalosporins, anti-pseudomonal carbapenems, combination beta-lactamase inhibitors, fluoroquinolones, or a combination of amikacin and third-generation cephalosporins.^{7,8, 21.} Aminoglycosides should be used cautiously in those with impaired kidney function.²¹ Fluoroquinolones should be avoided in patients with risk factors for quinolone resistance such as recent hospitalization, prior quinolone use, or urinary catheter presence.²¹Urine culture sensitivities can then be used to narrow the antibiotics that are continued for up to 6 weeks.^1,2,17

Additional treatment for EPN is controversial and urology consultants should be involved early on.¹⁹ Medical management includes antibiotics, IV fluid administration, and glucose control. When pursued alone, medical management is associated with worse outcomes and mortality rates approaching 75% in the past.^{1,19, 20} Most earlier cases therefore were treated with a combination of medical management and emergent nephrectomy or surgical drainage but there was still high mortality rate approaching 50%.²⁰Newer strategies now include the use of percutaneous drainage (PCD) along with appropriate medical management.^3,4,14,16,17 PCD with medical management is associated with the lowest mortality (13.5%) and is often the first line treatment for patients with localized infection with functional kidney tissue such as in Class 1 and Class 2.¹⁹ Patients with renal calculi often require PCD or stent placement.^5,16,18 Emergent nephrectomy may be pursued if patients fail PCD, or have multiple risk factors, a non-functioning kidney, significant parenchymal damage, or worse classifications such as Class 3A and 3B.^1,6,14,17 The treatment for Class 4 EPN is specialized. Those with bilateral EPN should be treated based on their overall presentation as well as the condition of each individual kidney. This may include a combined approach with medical management and a single emergent nephrectomy or possible bilateral PCN, for example.¹For solitary kidney EPN, preferred treatment is PCN combined with medical management in order to avoid lifeline renal replacement therapy. However, if the single kidney is nonfunctioning (ESRD), then emergent nephrectomy should be pursued.¹

Because of the overall high mortality and associated septic shock, many patients will require ICU level care.¹⁸

Case Resolution

The patient is septic, likely from a urinary source. She is started on piperacillin-tazobactam and IV fluids. Because of her CT findings demonstrating gas in the left renal parenchyma and extending to the perinephric space (Class 3A), urology is emergently consulted. The patient undergoes PCD and is admitted to the ICU for further management.

Key Points:

Suspect EPN in patients with risk factors (DM, immunocompromised, female sex) who present with fever/dysuria/abdominal pain or who do not respond to usual pyelonephritis treatment.
CT imaging of the abdomen and pelvis with contrast is the imaging modality of choice to identify gas. KUB or US may be used to aid in early recognition.
EPN has a high mortality rate. Start resuscitation measures early including empiric antibiotic therapy such as third-generation cephalosporins with aminoglycosides, fourth-generation cephalosporins, carbapenems, combination beta-lactamase inhibitors, or fluoroquinolones depending on patient risk factors (note: take into account local antibiogram).
Consult urology emergently to determine the need for further procedural interventions such as PCD or if severe/nonfunctioning, emergent nephrectomy.

References/Further Reading:

Pontin AR, Barnes RD. Current management of emphysematous pyelonephritis. Nature Reviews Urology. 2009;6(5):272-279. doi:10.1038/nrurol.2009.51
Deoraj S, Zakharious F, Nasim A, Missouri’s C. Emphysematous pyelonephritis: outcomes of conservative management and literature review. BMJ Case Reports. December 2018. doi:10.1136/bcr-2018-225931
Huang J-J, Tseng C-C. Emphysematous Pyelonephritis. Archives of Internal Medicine. 2000;160(6):797. doi:10.1001/archinte.160.6.797
Aboumarzouk OM, Hughes O, Narahari K, et al. Emphysematous pyelonephritis: Time for a management plan with an evidence-based approach. Arab Journal of Urology. 2014;12(2):106-115. doi:10.1016/j.aju.2013.09.005
Elawdy MM, Osman Y, Abouelkheir RT, El-Halwagy S, Awad B, El-Mekresh M. Emphysematous pyelonephritis treatment strategies in correlation to the CT classification: have the current experience and prognosis changed? International Urology and Nephrology. 2019;51(10):1709-1713. doi:10.1007/s11255-019-02220-3
Sokhal AK, Kumar M, Purkait B, et al. Emphysematous pyelonephritis: Changing trend of clinical spectrum, pathogenesis, management and outcome. Türk Üroloji Dergisi/Turkish Journal of Urology. 2017;43(2):202-209. doi:10.5152/tud.2016.14227
Lu Y-C, Chiang B-J, Pong Y-H, et al. Emphysematous pyelonephritis: Clinical characteristics and prognostic factors. International Journal of Urology. 2013;21(3):277-282. doi:10.1111/iju.12244
Shetty S. Emphysematous Pyelonephritis (EPN) Treatment & Management: Approach Considerations, Antibiotic Therapy, Percutaneous Drainage and Other Conservative Management. https://emedicine.medscape.com/article/2029011-treatment. Published December 5, 2019. Accessed May 24, 2020.
Mohsin N, Budruddin M, Lala S, Al-Taie S. Emphysematous Pyelonephritis: A Case Report Series of Four Patients with Review of Literature. Renal Failure. 2009;31(7):597-601. doi:10.1080/08860220903003396
Askew KL. Urinary Tract Infections and Hematuria. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e New York, NY: McGraw-Hill; http://accessemergencymedicine.mhmedical.com.eresources.mssm.edu/content.aspx?bookid=2353&sectionid=219643063. Accessed May 24, 2020.
Tonolini M. Imaging of Extrarenal Spread, Fistulising and Atypical Pyelonephritis. In: Imaging and Intervention in Urinary Tract Infections and Urosepsis. Springer International; 2018.
Peng C-Z, How C-K. Diagnostic Challenge of Emphysematous Pyelonephritis. The American Journal of the Medical Sciences. 2017;353(1):93. doi:10.1016/j.amjms.2016.03.002
Brown N, Petersen P, Kinas D, Newberry M. Emphysematous Pyelonephritis Presenting as Pneumaturia and the Use of Point-of-Care Ultrasound in the Emergency Department. Case Reports in Emergency Medicine. 2019;2019:1-5. doi:10.1155/2019/6903193
Somani BK, Nabi G, Thorpe P, Hussey J, Cook J, N’Dow J. Is Percutaneous Drainage the New Gold Standard in the Management of Emphysematous Pyelonephritis? Evidence from a Systematic Review. Journal of Urology. 2008;179(5):1844-1849. doi:10.1016/j.juro.2008.01.019
Wan YL, Lee TY, Bullard MJ and Tsai CC: Acute gas-producing bacterial renal infection: Correlation between imaging findings and clinical outcome. Radiology 1996; 198: 433.
Hinkamp CA, Keshvani N. Emphasising classification in emphysematous pyelonephritis. The Lancet. 2020;395(10230):1145. doi:10.1016/s0140-6736(20)30475-x
Turney JH. Renal conservation for gas-forming infections. The Lancet. 2000;355(9206):770-771. doi:10.1016/s0140-6736(99)00351-7
Elbaset M, Zahran MH, Hashem A, et al. Could platelet to leucocytic count ratio (PLR) predict sepsis and clinical outcomes in patients with emphysematous pyelonephritis? Journal of Infection and Chemotherapy. 2019;25(10):791-796. doi:10.1016/j.jiac.2019.04.008
Falagas ME, Alexiou VG, Giannopoulou KP, Siempos II. Risk Factors for Mortality in Patients With Emphysematous Pyelonephritis: A Meta-Analysis. Journal of Urology. 2007;178(3):880-885. doi:10.1016/j.juro.2007.05.017
Ubee, S.S., McGlynn, L. and Fordham, M. (2011), Emphysematous pyelonephritis. BJU International, 107: 1474-1478. doi:10.1111/j.1464-410X.2010.09660.x
Lu, Y., Hong, J., Chiang, B., Pong, Y., Hsueh, P., Huang, C., & Pu, Y. (2016). Recommended Initial Antimicrobial Therapy for Emphysematous Pyelonephritis. Medicine,95(21). doi:10.1097/md.0000000000003573

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EM@3AM: Marine Animal Bites and Stings

Sat, 26 Sep 2020 08:17:11 GMT

Author: Dustin Taliaferro, DO (Emergency Medicine resident, UT Southwestern, Dallas, TX) // Reviewed by: Cynthia Santos, MD (@Cynthia Santos, MD); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 30-year-old male presents to the emergency department with intense left forearm pain after cleaning an aquarium at his job 20 minutes prior to arrival. He is unsure what kind of fish were in the aquarium. The pain has been constant since onset. He does not endorse any nausea, vomiting, headache or weakness to his left arm. He denies any medical problems.

Initial vital signs: BP 122/82, HR 102, T 98.2 Oral, RR 16, SpO2 98% on RA. Physical exam reveals a patient who appears uncomfortable holding his left arm. He is A&OX3. His lungs and heart are normal. There is a 5 cm area of erythema to his anterior forearm that is warm to the touch. Radial pulses are 2+.

What is the diagnosis and the best next step in management?

Answer: Marine animal injury; treatment – hot water immersion

Background: Human contact with species of venomous marine life are relatively common especially in tropical and coastal regions of the world. Common organisms include spiny fish, cone snails, jelly fish, sea snakes, octopi and stingrays. There is an estimated 10 million envenomations worldwide, most being caused by jellyfish. Most of these animals do not inhabit US waters. It is important to know what the common organisms are based on region to determine if an envenomation can be potentially fatal. While most of these envenomations are relatively mild, there are fatal organisms that are most commonly in Australian and Pacific waters.

Envenomations can be broken down into three classes based on mechanism of delivery: stingers, nematocysts and bites

Stingers

Rays: Rays are a member of the class Chondrichthyes. Families in this class include sting rays, whip rays, skates, round rays, eagle rays, butterfly rays and freshwater rays. There are 11 different species of sting rays in US coastal waters. It is estimated that 1500 to 2000 ray injuries occur in the US every year. A majority of these injuries occur when the ray is stepped on. Deaths from these envenomations typically occur from hemorrhagic abdominal trauma, organ puncture or tetanus.

Envenomation:
- Rays possess a tail that is covered with retroverted spines. There is a ventrolateral groove that contains venom and saturates the spines. The venom is made up of heat labile polypeptides. The ray venom causes local vasoconstriction that can cause necrotic tissue. Typically, a single puncture wound is found on the top or side of the foot. Stepping on a ray causes the ray’s tail to whip and contact the person. Intense pain out of proportion to the wound is usually observed. Peak onset of symptoms is 30 to 90 minutes after initial injury and may last for 48 hours. Wounds may progress to a hemorrhagic necrosis and possibly necrotizing fasciitis.
- Symptoms from the venom cause weakness, nausea, vomiting, diarrhea, headache, syncope, seizures, muscle cramps, hypotension and dysrhythmias.
Management:
- Radiographs for retained spine
- Wound irrigation, tetanus prophylaxis
- Consider antibiotics covering skin flora and aquatic organisms
- Hot water immersion (43C-45C) relieves pain and inactivates venom
- Observe for 3-4 hours for systemic symptoms
Disposition:
- Discharge if no systemic symptoms after 2 hours of observation
- Admit for compartment syndrome, skin necrosis or NSTI

Bony Fish: Bony fish are classified under the family Scorpaenidae have several venomous species. Some of the more common species include lionfish, stonefish, scorpionfish, weevers and catfish. People at high risk for these envenomations include fishermen, waders and aquarium handlers. There are very few deaths associated with Scorpaenidae with only five reported. Scorpaenidae have 12-13 dorsal, 2 pelvic and 3 anal spines covered by an integumentary sheath. Stings occur from direct contact with spines on the fish. Venom from these spines can remain toxic for 24-48 hours even after death.

Lionfish and Scorpionfish: These stings are common in aquarium enthusiasts. They are the most common poison center call for bony fish stings in the US. Due to their popularity in the US, Lionfish have become an invasive species in US Caribbean waters. They have no known natural predators which allows them to thrive and disrupt coral ecosystems. Immediately following a sting, the victim experiences intense pain and if left untreated can last up to 48 hours. The area becomes warm, erythematous, and edematous with vesicles.

Stonefish: Stonefish are commonly found in coastal Australia. They are disguised to accommodate living on the rocky sea bottom. Stings from stonefish are the most severe in this category. The area of the sting becomes immediately painful and erythema can progress up the effected extremity. Although pain typically subsides in 6-12 hours, it can last for several days. Signs of systemic toxicity include headache, vomiting, abdominal pain, delirium, seizures, limb paralysis, arrhythmia, congestive heart failure and hypotension.
Weevers: Weever stings are common in Italian coastal towns. They inhabit shallow temperate waters in the eastern Atlantic and Mediterranean.
Catfish: Most species of catfish live in freshwater but marine catfish that can inflict injury inhabit tropical Indo-Pacific waters.
Management:
- Management for all bony fish is centered around hot water immersion to inactive venom, removal of retained spines and pain control
- Copious wound irrigation and inspection/radiographs for retained spines
- Oral analgesia and local injection of lidocaine for pain
- Consider antibiotic prophylaxis with coverage for vibrio parahaemolyticus such as doxycycline, trimethoprim-sulfamethoxazole, third-generation cephalosporins (cefotaxime and ceftazidime), aminoglycosides (gentamicin and amikacin) and fluoroquinolones
- Address tetanus immunization status
- There is an antivenom for stonefish stings that is used for systemic symptoms or pain refractory to first aid
- Observe for anaphylactic reaction to antivenom
Disposition:
- Discharge after 2 hours observation if no systemic symptoms
- Stonefish envenomations will need ICU level care if systemic symptoms

Echinodermata, Annelida, and Porifera: The Echinodermata phylum include sea stars, sea urchins, sand dollars and sea cucumbers. The Annelida phylum include segmented worms such as the bristle worm. The Porifera phylum include sponges. These are slow moving or sessile creatures that live on the ocean floor where envenomation happens passively by people stepping on the animals or mistakenly handling them.

Echinodermata
- Sea urchins are covered in spines and pedicellariae (pincer-like appendages used for feeding, cleaning and defense). Wounds with more pedicellariae are generally more severe due to the pedicellariae containing more venom and being harder to remove. The venom found in sea urchins consist of steroid glycosides, serotonin, hemolysin, protease and acetylcholine-like substances.
  - Most injuries from sea urchins are mild. Burning with local irritation and erythema occur at the site of envenomation. A Pacific Ocean urchin, Tripneustes, has a neurotoxin that can affect cranial nerves.

- Sea star envenomations are usually less severe than urchins due to sea stars having short and blunt spines. The Crown-of-Thorns sea star has longer spines that contain a toxic saponin venom with hemolytic and anticoagulant properties.
  - Small cuts on the foot or hands from sea stars can lead to contact dermatitis. The Crown-of-Thorns species may cause nausea, vomiting and muscle paralysis.
- Sea cucumbers excrete holothurin from their anus as a defense mechanism. This toxin inhibits neural conduction in fish. Sea cucumbers can also eat jellyfish and subsequently excrete their toxin.
  - Contact with sea cucumbers cause a mild dermatitis. Scleral or corneal contact can cause several corneal inflammation and blindness.
Annelida
- Bristle worms have stingers that project from pseudo legs. They excrete an unknown venom.
  - Contact with the bristles of bristle worms cause a mild urticarial rash.
Porifera
- Sponges attach to the sea floor or other coral and have elastic skeletons with projecting spicules. These spicules contain a halitoxin, okadaic acid and subcritine. Dried sponges are nontoxic but can produce toxin upon rewetting, even after years.
  - Contact with certain species of sponges can cause a rash with vesicles and bullae. These symptoms usually subside within a week with skin desquamation occurring from 10 days to 2 months. Skin changes can last from months to several years. Sponges colonized with Cnidaria spp. can lead to skin necrosis (sponge diver’s disease).
Management:
- Particularly for urchins and sea stars, the primary objective is venom inactivation by hot water immersion
- Irrigate sponge envenomations with cold water
- Pain control
- Radiographs to evaluate for foreign bodies
  - Some urchin species have spines that contain dyes that may resemble a foreign body
- Spicule removal from sponges by adhesive tape or edge of a credit card
- Antihistamine and steroid creams may provide some relief for itching
- Consider antibiotics for severe wounds that cover skin and aquatic flora
Disposition:
- Discharge after 2-hour observation period if no systemic symptoms

Cone Snails: Cone snails are cone-shaped with a broad conical spire at the apex. They belong to the genus Conus with about 400 species totaling in the genus. 18 of these are known to be venomous to humans. There are a reported 15 human deaths associated with cone snail stings. The fish hunting cone is the species that is most implicated in human envenomations. Envenomations typically occur when they are handled.

Envenomation: Cone snails have a long hollow tube (proboscis) that contains a single tooth bathed in venom. When the snail detects nearby prey, the tooth is fired from the proboscis into the victim. Some specie’s venom contains a vasopressin-like peptide that is used in medical pain control for its antinociceptive properties. Cone snail stings can be very severe. The venom causes local inflammation, intense pain, tissue cyanosis and numbness. Systemic symptoms include weakness, blurred vision, aphonia, dysphagia, muscle paralysis, muscle paralysis, respiratory failure and cardiovascular collapse. Death is rapid and occurs within two hours.
Management:
- Cone snails are widespread throughout the world, including off the Atlantic Coast of Florida. Consider these injuries in divers handling wildlife
- Airway management
- Supportive care
- Hot water immersion for pain control
- Pressure immobilization is controversial
- Tetanus prophylaxis
Disposition: Patients without systemic signs of toxicity at 4-6 hours can be discharged. Symptoms typically take 3 days to fully recover.

Nematocysts

Nematocysts (Cnidarians): The Cnidaria phylum consist of true jellyfish, cubozoans (box jellyfish) and Physalia (Portuguese Man-of-War), sea anemones and coral. Organisms from this phylum are invertebrates that are the leading cause of lethal envenomations from marine animals worldwide. While most envenomations are nonlethal, injuries from the box jellyfish can be fatal.

Cubozoans (box jellyfish)
- Chironex fleckeri: C. fleckeri are a species of box jellyfish that can cause cardiac arrest within minutes. They have a unique sting pattern known as the “frosted ladder” pattern that appears in a cross-hatch pattern. C. fleckeri are found in Australia and Indo-Pacific waters. Death is usually immediate within 5-20 minutes. Antivenom is needed immediately but there is controversy over efficacy.

- Carukia barnesi (Irukandji jellyfish): C. barnesi are characteristic in causing Irukandji Syndrome. This syndrome is characterized by muscle cramps, severe back pain, burning sensation to skin and face, headaches, nausea, restlessness, sweating, nausea, hypertension and tachycardia. Irukandji Syndrome is mediated by a catecholamine release from exposure to the toxin. C. barnesi have small bells with small tentacles. They do not leave typical serpiginous wounds on contact. This species is typically limited to Australia and the Indo-Pacific, although cases have been reported off the coast of Florida.
Physaliidae: Members of the Physaliidae family are of the Hydrozoa class and, like the Cubozoans, are not true jellyfish. These organisms exist as floating colonies meaning the bells and tentacles are actually different organisms. They are recognized by a blue sail that floats on the surface of the water.
- Physalia physalis is known as the Portuguese man-of-war and are found on Atlantic coastlines, especially in Florida. These envenomations are common among beachgoers on the Atlantic Florida beaches. Their tentacles can reach lengths of 30 meters and contain over 750,000 nematocysts on each tentacle (up to 40 tentacles).

Physalia utriculus is known as the blue bottle and are found in Indo-Pacific waters. They contain only one tentacle that can reach 15 meters in length.
- The most common reactions from these toxins include intense pain with burning and redness at the site. There have been reports of wounds severe enough requiring skin grafts. Systemic signs include anaphylaxis, headache, vomiting, abdominal pain and diarrhea. Death is extremely rare.
Scyphozoa are the class of true jellyfish. Jellyfish species are diverse in shape, color and size. Common jellyfish that are known to envenomate are the hair jelly, sea nettle and mauve stinger. The mauve stinger is well known as it is pink during the day and phosphorescent at night.
Envenomation: Envenomation from Cnidaria occur from persons coming into contact with tentacles. The tentacles are lined with nematocysts (cnidae). Envenomation is typically inadvertent from swimmers coming into contact with them. Mechanical stimulation of the tentacles causes cnidae to discharge venom. The venom is consisted of various neurotoxins, myocardial toxins, vasodilatory toxins (histamine and serotonin), proteolytic and lipolytic enzymes and membranotoxic pore-forming complexes. It is estimated that less than 1% of cnidae discharge venom on initial contact. Subsequent discharge of cnidae is caused by pouring freshwater on or trying to take off the tentacles. Most of these injuries are non-life threatening. Stinging and burning occur immediately. Skin changes range from urticaria to bullae and skin necrosis. Whip-like lesions may not appear for several minutes to hours.
Management:
- Address ABCs
- It is critical in reducing venom load and reducing venom exposure by removing tentacles
- It is important to know which species inhabit the region the victim is in. Box jellyfish only inhabit Australian waters so for an envenomation in the US, antivenom does not need to be considered. Stings regionally in the US are likely to be from less lethal species such as Portuguese man-of-war
- Antivenom for box jellyfish should be administered immediately if possible
  - IV magnesium can be given if no response to antivenom
- Irukandji Syndrome can be fatal. Use benzodiazepines for hypertension, agitation and tachycardia. Consider nitroglycerine or phentolamine drips for refractory symptoms.
- 100% vinegar for 30 seconds should be applied first to irreversibly inhibit nematocyst discharge
- Tentacles should be picked off, not scraped. Scraping can lead to increased nematocyst discharge
- Methods that increase nematocyst discharge and should be avoided are rinsing with freshwater, urine, ethanol and ammonia
- Saltwater rinses are not recommended as it can discharge nematocysts by mechanical force
- Topical lidocaine is not recommended as it can increase nematocyst discharge
- Hot water has been shown to significantly reduce pain
Disposition:
- If systemic or severe symptoms, patient will need admission
- Discharge if no systemic symptoms
Fire Coral
- The fire coral (Millepora alcicornis) is different than other members of the Cnidaria class as it is sessile and exists as a fixed colony of hydroids. It appears like normal coral and has a white to yellow or green exoskeleton. Small tentacles (dactylozooids) protrude through small gastropores in the exoskeleton. The venom contains in the nematocysts have hemolytic, dermonecrotic and cytotoxic toxins. Fire corals are widespread and exist in throughout the world with most victims being snorkelers and scuba divers.

- Lacerations are associated with fire coral injuries due to their rigid structure. Envenomation occurs immediately and results in intense pain, pruritis and urticaria. Blistering occurs up to 6 hours after exposure. Pain and sensitivity can last for months after exposure. Systemic symptoms are extremely rare.
- Management:
  - Fire coral are found throughout the world. Consider these injuries in swimmers and divers.
  - Oral analgesics, topical lidocaine and steroids may help symptoms
  - Hot and cold water equally efficacious for pain with irrigation
  - Lacerations should be copiously irrigated and loose closure
  - Antibiotics covering skin and aquatic flora
  - Tetanus prophylaxis
- Disposition:
  - Symptoms are usually localized to the skin. Patient can be discharged if no systemic symptoms.
Sea anemones
- Sea anemones are in the class Anthozoa and are considered venomous carnivores. Anemones have tentacles that are coated in toxins that inactive voltage gated sodium channels causing paralysis to victims. Anemones have modified nematocysts called sporocysts. These envenomations are typical in persons swimming around coral reef without protective suits.
- Management:
  - Due to the neurotoxic nature of the venom, manage ABCs extremely closely
  - Deactivate sporocysts with vinegar
  - Hot water immersion of injured extremity for up to 90 minutes
  - Oral or IV analgesia
  - General wound care and consider antibiotics that cover aquatic species and skin flora if wound appears infected
  - There is no antivenom available
- Disposition:
  - Symptoms are usually mild and localized to skin lesions. Patient can be discharged if no systemic symptoms.

Bites

Octopus

Background: Octopuses are of the phylum Mollusca and the Cephalopoda class. The cephalopod of greatest toxicologic concern is the blue-ringed octopus. Blue-ringed octopuses are typically found in Australia. Most bites from these animals come from being handled out of water. When agitated, their bodies darken, and their blue circles become iridescent blue.
Envenomation: The beak of the octopus creates small puncture wounds in which the venom is introduced. Bites may be painless and symptom onset is within 10 minutes. One of the toxins found in blue-ringed octopus’ venom is identical to tetrodotoxin. Tetrodotoxin blocks fast sodium channel conduction ranging from a tingling sensation around the mouth to flaccid muscle paralysis. Death results from respiratory failure and hypotension. Patients may need ventilatory support from 6 hours to several days.

Management:
- Fatal octopus bites are only found in Australia
- ABCs; intubate if respiratory failure
- No antivenom available
- Consider pressure bandage immobilization
- Wound care, tetanus prophylaxis
Disposition:
- ICU care for ventilatory support
- Prognosis is good even with artificial respiratory support
- If no paralysis, patient can be discharge after an observation period of 4-6 hours
- Delayed hypersensitivity can occur
- Joint pain can persist for weeks

Sea snakes

Background: Sea snakes are front fanged venomous reptiles that are closely related to the cobra and krait. Their bodies are flattened and brightly colored. They are distinguished from eels by the presence of scales and the lack of gills and fins. All 52 species of sea snakes are venomous with the most common being the baked sea snake and the yellow-bellied sea snake. Sea snakes are common in Australia, Pacific Ocean, Indian Ocean and the Persian Gulf. Hawaii is the only US state where sea snakes inhabit. They are usually docile except when threatened or during mating season. Fishermen and waders are people at most risk.
Envenomation: Bites range from painless to mild discomfort. 1-4 fang marks are common but over 20 can be found with multiple bites. Sea snake venom contains neurotoxic and myotoxic proteins. Some venoms contain nephrotoxins associated with acute renal tubular degeneration, proliferative glomerulonephritis and liver failure. Venom from sea snakes is generally more lethally potent than terrestrial snakes. Myotoxic venom results in rhabdomyolysis, painful muscular rigidity, myoglobinuria and skeletal muscle paralysis. These are hallmarks of sea snake envenomations. The neurotoxic component results in an ascending muscle paralysis, dysarthria, dysphagia, ptosis and airway compromise.
Management:
- Bite marks may not be apparent. History and presenting symptoms are vital
- Symptom onset is within 4 hours
- ABCs
- If respiratory failure and/or rhabdomyolysis, give antivenom
  - CSL sea snake antivenom is first line starting with 1-3 vials, max 10, if severe symptoms
  - CSL tiger snake antivenom can be used if sea snake antivenom unavailable
    - 1 vial sea snake antivenom=2-4 vials of tiger snake antivenom
  - Neostigmine and atropine can be considered if no antivenom available although there is no evidence to evaluate efficacy
- Electrolytes, creatinine, CK, urinalysis to assess for the presence of renal failure, rhabdomyolysis, myoglobinuria and hyperkalemia
- EKG
- Do not wash wound
- Apply PBI if no antivenom available
- IV fluids for rhabdomyolysis
Disposition
- Patient can be discharged if no symptoms within 2-4 hours (“dry bite”)
- Consider ICU level care for symptomatic patients
- If given antivenom, education on serum sickness 4-14 days after therapy needs to be given

A 26-year-old man presents to the emergency department with severe finger pain after accidentally touching a lionfish in his saltwater tank while cleaning the glass. He is afebrile, and the remainder of his vital signs include a heart rate of 101 beats per minute, blood pressure of 128/91 mm Hg, respiratory rate of 19 per minute, and a room air pulse oximetry reading of 100%. Examination is remarkable only for mild erythroderma at the site of his pain, where he reports touching the fish. Which of the following therapies is most appropriate?

A) Acetic acid application

B) Cold-water immersion

C) Hot-water immersion

D) Salt water immersion

E) Topical calcium gluconate

Answer: C

Human contact with venomous marine creatures, both in nature and captivity, is common. Serious harm can result from biologic toxins or mechanical trauma inflicted by the stinging apparatus. Common venomous aquatic organisms include the phylum Cnidaria (anemones and jellyfish), Mollusca (octopods and snails), Echinodermata (sea urchins and sea stars), Hydrophiidae (sea snakes), and various spined fish. The lionfish (Pterois spp) is a spiny fish of the family Scorpaenidae and is often kept in home saltwater tanks. Lionfish possess dorsal, anal, and pelvic spines that are linked to venom glands, so the pressure applied topically to the spine is proportional to the amount of venom released. The venom contains a variety of compounds that cause immediate–onset pain, erythroderma, and swelling. Local symptoms are effectively treated with hot-water immersion. This is performed by immersing the envenomated site at 45°C for 20 minutes. Additional cycles of hot-water immersion can be performed if necessary secondary to persistent discomfort. Patients occasionally require a single dose of oral or parenteral analgesia, however, these are infrequently required upon discharge. The organism’s spine often breaks off in the wound, therefore, radiography and ultrasound should be performed to investigate the possibility of retained foreign bodies. Tetanus immune status should be addressed, and prophylactic antibiotics (including cefazolin and a quinolone) have been shown to decrease the rate of wound infection.

Topical acetic acid application (A) is a common first-line treatment for jellyfish stings. Jellyfish possess microscopic cnidae (“nettles”), which are specialized organelles consisting of a barbed thread bathed in venom. Release of this whiplike structure is controlled by a cnidocil. Cnidae are organized into nematocysts and distributed along the jellyfish’s tentacles. These discharge and release venom in response to changes in physical pressure (from contact with a victim’s skin) or osmolarity. The osmolarity of acetic acid, particularly in vinegar, is similar to that of seawater and, therefore, causes a decrease in venom release. Cold-water immersion (B) is not nearly as effective as hot-water immersion in treating lionfish envenomation. Many marine venoms are heat labile and denature or otherwise neutralize at supraphysiologic temperatures. Saltwater immersion (D) of the affected digit would be useful in jellyfish envenomation for the same reasons as acetic acid. Topical calcium gluconate (E) has been reported to be effective in treating dermal hydrofluoric acid exposures, but it plays no role in the management of marine envenomations.

Rosh Review Free Qbank Access

Trauma ICU Rounds – Endpoints of Resuscitation

Fri, 25 Sep 2020 17:40:23 GMT

Originally posted on Trauma ICU Rounds on April 24, 2020. Follow Trauma ICU Rounds (@traumaicurounds) and Dr. Kim (@dennisyongkim) to learn more on simplifying trauma critical care together.

Summary

Before the COVID19 pandemic hit the US and California became the first state to issues Stay Safe at Home orders, I had an opportunity to meet with Dr. Matt Martin from Scripps Mercy Hospital in San Diego at the 91st Annual Pacific Coast Surgical Association (PCSA) Meeting in Carlsbad, CA (Feb. 14-17, 2020) for our first interview on Rounds.

During the course of our discussion we reviewed several recent changes in our resuscitation strategy of injured patients. We also discussed endpoints of resuscitation and emphasized the need to first, understand the clinical problem in need of resuscitation and, second, identify the targets or goals of resuscitation.

Learning Objectives

By the end of Rounds, you should have an appreciation of:

The initial assessment of critically ill and injured patients.
Methods for identifying the presence or absence of shock
Various modalities for identifying patients in need of resuscitation

Take Home Points

Always start your assessment by asking yourself, “What’s going to kill my patient immediately?” This question is followed by, “What common problems or clinical diagnoses should I rule out?”. Only then should you start thinking about zebras.
Whole blood is the best individual fluid you can give. Consider a plasma first resuscitation strategy in bleeding trauma patients.
Every time you assess a patient, classify them as being either “sick” of “not sick”.
Resuscitation endpoints should be tailored on the basis of what condition is in need of resuscitation AND identifying not just our endpoints but where are we in terms of start points.

Time Stamps

00:13 Introduction
01:39 Military Experience – Pre-hospital & In-hospital Assessment
04:03 Resuscitation Fluids & Whole Blood
06:08 Endpoints in Patients with Suspected TBI
07:28 Shock Index, Narrowed Pulse Pressure
09:42 Whole Blood Resuscitation
11:44 Pre-hospital biomarkers (POC lactate)
13:45 StO2 Monitoring
14:53 Permissive Hypotension following Penetrating Torso Trauma
16:50 Popping the Clot
18:11 Matt Martin’s Approach to the “Sick” vs. “Not Sick” Trauma Patient
23:05 ACS Classification of Hemorrhage
24:06 Utility of Urine Output Monitoring in “Sick” Patients
25:47 Utility of Lactate & Base Deficit
27:49 Lactate Clearance & Touching on Type A vs. Type B Lactic Acidosis
29:28 Over-Resuscitation & the “Lactobolus Reflex”
31:31 A Normal Lactate Means Nothing in Mesenteric Ischemia
34:06 Application of Ultrasound during Active Resuscitation of Critically Ill Patients
39:54 CVP Sucks
40:34 Final Messages
42:30 Outro

Potential Indicators of the Need for Transfusion or Emergent Hemorrhage Control Intervention

Shock Index (SI) = HR / SBP (HIGH SI defined as >0.8)

Narrow Pulse Pressure (PP) <=30 mmHg (varies with age)

Assessment of Blood Consumption (ABC) Score

Penetrating mechanism
Arrival systolic BP 90 mmHg or less
Arrival heart rate > 120 bpm
+ FAST

*score <2, unlikely to require massive transfusion; sensitivity (75 – 90%) & specificity (67 – 88%)

ACS Classification of Hemorrhagic Shock

Regarding the classification of hemorrhage shock, always start with the patient’s vitals. The finding of a narrow pulse pressure should alert you to the potential for bleeding. For example, if a patient arrives following a GSW to the abdomen and the initial BP reads 140/115, this should not be interpreted as normal!!!! In hemorrhagic shock, the loss of intravascular volume results in decreased preload, stroke volume, and cardiac output.

Remember the mean arterial pressure (MAP) is the product of cardiac output (Q) & systemic vascular resistance (SVR). If cardiac output is decreased due to a decreased stroke volume, the body will attempt to compensate by increasing vascular tone. This may manifest as an elevated diastolic pressure or a narrow pulse pressure. Check out a study we published on this topic listed in the Recommended Reading below.

Mental status or GCS is a readily accessible and quick measure of the presence or absence of hypoxic encephalopathy. Although many confounders may alter the exam (TBI, alcohol, drugs, etc.) an altered mental status should always alert you tot he presence of brain hypoxia. In the setting of trauma the number 1-2-and3 causes of shock are BLEEDING-BLEEDING-BLEEDING!!!

For patients recognized as being in shock, immediate intervention is required followed by REASSESSMENT & REEVALUATION. Every intervention should be immediately followed by asking if patients have a desired response. Patients typically respond in 1 of 3 ways. They may RESPOND. They may TRANSIENTLY RESPOND or they may NOT RESPOND. In the latter 2 cases, you should have a very low threshold for transfusing blood & blood products NOT salt water!!!!

History of EM Series: Benson Munger

Thu, 24 Sep 2020 23:27:06 GMT

Author: Benson Munger, PhD (founding Executive Director of the American Board of Emergency Medicine, https://www.linkedin.com/in/bensonmunger/) // Reviewed by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Emergency Medicine is an amazing specialty, but how did it develop, and where do we go from here? This new series looks at these questions and more with write-ups from the masters of our field.

Why EM then?

Emergency Medicine was a classic example of a patient-driven specialty. At the end of the Vietnam War, there were few Emergency Departments as you currently think of them. As patients began to expect a higher level of care there developed a group of physicians who saw that need and began to work with hospitals to fill it. This was happening at a time when physicians were beginning to see the advantages of a group practice. In retrospect, the movement to the adoption of Emergency Departments as we currently know them was very rapid and particularly when hospitals understood its implications to address many of their administrative issues.

Most interesting personal EM story and tidbit of EM history…

From the inception of ACEP’s identification of specialty status through the American Board of Medical Specialties (ABMS), the goal was a primary board, equivalent to the existing 22 primary boards such as Surgery, Pediatrics, etc. The College expended dues, raised voluntary contributions and organized their strategy toward that end. The first and overwhelmingly negative vote in ABMS was a complete rejection. Certification is at its core an academic process. It addresses the way physicians are trained in a specialty and defines the relationship among the primary specialties. In the late 1970s, the other 22 primary boards had control of the Emergency Departments in academic medical centers and they were unwilling to cede control of those spaces for training their residents.

At that vote, it was obvious to everyone that the current mindset had to change. The current Executive Director of ABMS, Glen Laymaster, called a meeting in Chicago of all primary boards with a stake in Emergency Medicine. At that meeting, there was a lot of discussion of the need for Emergency Medicine to reside within the other primary specialties. Clearly the other primary specialties saw Emergency Medicine as important but as subordinate. In historical context, it was critical that the ABMS has not yet conceived of the idea of a joint subspecialty that would reside in multiple primary specialties, something that exists today.

At a particularly important part of the Chicago meeting. Dr. John Wiegenstein asked each of the other primary boards to outline the training in their specialty they felt would be required. By the time the group was finished the number of years exceeded 20. From the end of that exercise, the concept of Emergency Medicine as a subspecialty was never raised again and the discussion moved rapidly toward the unique solution that created the path for Emergency Medicine to eventual certification as the 23rd primary board in medicine.

The post History of EM Series: Benson Munger appeared first on emDOCs.net - Emergency Medicine Education.

ToxCard: Green Urine?

Tue, 22 Sep 2020 07:15:50 GMT

Authors: Chelsea Wilson, MD (Emergency Medicine Resident, Carolinas Medical Center, Charlotte, NC); Kathryn T Kopec, DO (Emergency Medicine Attending; Medical Toxicologist, Carolinas Medical Center, Charlotte, NC) // Reviewed by: Cynthia Santos, MD (@Cynthia Santos, MD); Alex Koyfman, MD (@EMHighAK); and Brit Long, MD (@long_brit)

Case:

A 47-year-old male presents to the emergency department (ED) following an ingestion of a pesticide he has on his farm. A bedside test is performed and is positive, shown in the photo.

What is the pesticide?

A) Paraquat

B) Malathion

C) Diquat

D) Glyphosate

Answer: C – Diquat, hence the topic of this post

What is Diquat?

Diquat (1,1’-ethylene-2,2’-bipyridinium ion) is a bipyridyl compound that is a nonselective herbicide. [1] It was first introduced in 1958 and is most heavily used in Asia. It is in the class of quaternary ammonium salts which includes another important herbicide, such as paraquat. [2] It can be used alone in salt or liquid form or in combination with other herbicides. Toxicity is mostly due to intentional ingestion for suicide attempts. [3] However, it is a rare form of poisoning with only around 75 cases reported in the medical literature. [2]

How does it cause damage?

Diquat is an odorless compound that is yellow when in solid form. It is poorly absorbed via all routes of exposure; however, highest rates of absorption are with direct injection (SQ), oral ingestion (~ 10%), followed by dermal and inhalation exposures. [2] The most common concentration is 20% and only requires 15ml to be lethal. Peak toxicity is about 2 hours after ingestion. [2,4]

Mechanism of Toxicity:
- Occurs thru redox cycling, an enzyme mediated process that forms reactive oxygen species (ROS) and depletion of reduced NADPH. [2]

- These ROS lead to damage of polyunsaturated fatty acids, used in cell membranes, which results in increased cell permeability causing membrane rupture and cell death. [2]

- Significant neurotoxic effects likely due to accumulation in neuromelanin nerve cells, which cause degeneration of dopaminergic neurons.
  - One pathognomonic effect seen with diquat toxicity is brain stem infarcts, which particularly affects the pons. [1]
  - This neurotoxic effect is substantially worse than paraquat due to diquat’s higher reduction potential resulting in a more rapid redox recycling process and a higher number of ROS in the CNS. [2]

Diquat is a hydrophilic molecule which causes it to have difficulty crossing membranes which results in high levels accumulating in the liver, kidneys and gastrointestinal tract. Unlike paraquat, which reaches high levels of concentration in the lungs, diquat has significantly lower concentrations found in the lungs secondary to not have any uptake by the polyamine system. [1] Elimination is mainly by excretion of the unchanged form in the stool (90-94%). [2]

Absorbed diquat is metabolized into its less toxic form of mono and dipyridone derivatives via the liver and the cytochrome P450 enzyme pathway and is then excreted in the urine.

Clinical Presentation:

Ingestion often presents with irritation, burning, or hemorrhagic ulcers of the oropharynx. [3]
Dermal exposure causes localized reactions of erythema, hyperkeratosis, and akathisia. [3, 4]
Almost universally and the key finding in diquat toxicity is renal damage.
- This can include ATN, proteinuria, anuria, and ARF. [1]
- Renal damage occurs regardless of the dose as the kidneys are the primary pathway for excretion of diquat.
CNS effects can include nervousness, irritability, decreased reflexes, disorientation, seizures, and coma. [2]
Once exposure occurs the clinical picture depends on the amount of diquat absorbed. [2]
- Mild exposures (< 1g)
  - Primarily gastrointestinal symptoms (nausea, vomiting, diarrhea, hematemesis)
- Moderate poisoning (1 – 12g)
  - Causes multiorgan failure (liver failure, kidney failure, CNS disturbances)
  - Two thirds of patients recover
- Severe poisoning (> 12g)
  - Progressive multi-organ failure and death.

Diagnosis:

As this is an extremely rare cause of poisoning, obtaining a good history is imperative to considering this diagnosis.
Urine Testing: Sodium Dithionite Test [1,2,4]

- Take 1 gm of sodium dithionite and 1 gm of sodium bicarbonate mixed with 10ml of patient urine.
- Positive = Green coloration
- Paraquat creates a blue coloration
- Depth or intensity of the color is dose related.
  - A darker green is associated with a higher level of exposure.
  - Strong/dark green color 4 hours post ingestion is consistent with a poor prognosis.
- Negative urine dithionite test 6 hours after ingestion suggests minimal exposure, and the patient can be medically cleared if asymptomatic.

Test rarely performed in the clinical setting include spectrophotometry, luminescences, quantum dots and gas chromatography. [2]
Additional workup involves evaluating toxic organ effects with a CBC, CMP, EKG and CXR on initial presentation. [1,2]

Treatment:

Focus of treatment is to minimize absorption of the diquat if possible. [1, 2, 3]
Mainstay is supportive care.
Dermal or ocular exposures should have contaminated clothing immediately removed and have copious irrigation of skin and / or eyes. [3]
For ingestions, priority should be placed on limiting absorption by administration of activated charcoal, Fuller’s earth, or Bentonite within 1 hour after ingestion. [3]
Avoid placing patients on supplemental oxygen unless hypoxic as high concentrations of oxygen could cause more injury due to increased ROS. [2]
- This data is extrapolated from paraquat treatment but is still recommended for diquat toxicity.
IVF resuscitation to maintain a normal urine output and adequate intravascular volume.
Diquat toxicity is associated with a high rate of renal failure, so careful attention should be paid to ensure the patient does not develop fluid overload. [2]
No role for forced diuresis or hemodialysis as they do not aid with elimination. [3]
- However, hemodialysis may be required secondary to acute renal failure.
A review in 2018 of diquat poisoning showed that out of the 74 cases currently in medical literature 31 were fatal, demonstrating a 41% mortality rate for the recorded cases. [2]

Take Home Points:

Diquat is a bipyridyl compound used as an herbicide and is a rare form of poisoning.
Poorly absorbed by all routes of exposure with oral ingestion having approximately 10% absorption with peak toxicity 2 hours after ingestion.
Toxicity occurs through redox cycling which produces ROS that depletes NADPH and breakdown of cell membranes.
Damage occurs in the central nervous system (irritability, seizures, brain stem infarct), gastrointestinal tract (nausea, vomiting, ileus), cutaneous (localized irritation, burn), kidneys (ATN, anuria and ARF) and liver (elevated LFT’s).

- Mild exposure < 1g result in primarily GI symptoms)
- Moderate exposure (1 – 12g), result in multiorgan failure
- Severe exposure > 12 g cause progressive organ failure and death

Diagnosis is made by history and urine sodium dithionite test with green coloration (dose related color intensity) of the urine.
Negative urine dithionite test 6 hours after ingestion suggests minimal exposure and the patient can be medically cleared if asymptomatic.
Treatment is focused on minimizing absorption by decontamination and administration of activated charcoal within 1 hour.
Supportive care with IV fluids to help maintain normal urine output, however caution should be used to prevent fluid overload due to high rate of renal failure.

References:

Roberts, J. R., & Reigart, J. R. (2013). 12. In Recognition and management of pesticide poisonings (pp. 110-117). Washington, DC: United States Environmental Protection Agency, Office of Pesticide Programs.
Magalhães, N., Carvalho, F., & Dinis-Oliveira, R. (2018). Human and experimental toxicology of diquat poisoning: Toxicokinetics, mechanisms of toxicity, clinical features, and treatment. Human & Experimental Toxicology, 37(11), 1131-1160. doi:10.1177/0960327118765330
Jones, G. M., & Vale, J. A. (2000). Mechanisms of Toxicity, Clinical Features, and Management of Diquat Poisoning: A Review. Journal of Toxicology: Clinical Toxicology, 38(2), 123-128. doi:10.1081/clt-100100926
Clark, D. G., & Hurst, E. W. (1970). The toxicity of diquat. Occupational and Environmental Medicine, 27(1), 51-55. doi:10.1136/oem.27.1.51

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