Tag Archives: #FOAM

MEDICAL MALPRACTICE INSIGHTS: Don’t miss a posterior shoulder dislocation

Author: Chuck Pilcher, MD, FACEP (Editor, Med Mal Insights) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

Here’s the second monthly post from Medical Malpractice Insights – Learning from Lawsuits, a free monthly opt-in email newsletter. The goal of MMI-LFL is to improve patient safety, educate physicians and reduce the cost and stress of medical malpractice lawsuits.

Chuck Pilcher MD, FACEP, Editor, Med Mal Insights

Don’t miss a posterior  shoulder dislocation

Critical thinking makes the diagnosis easy

Facts: A 42 yo well-dressed businessman presents to the ED with pain in his left shoulder after slipping and falling on his outstretched arm on a wet sidewalk about 2 hours earlier. He has no prior history Screen Shot 2017-02-16 at 9.31.17 PMof shoulder problems. Exam shows very limited and painful ROM with the shoulder held in adduction and internal rotation. There is a normal appearing “deltoid bulge” indicating no anterior dislocation. An impacted humeral head fracture is suspected. An x-ray is read by both the ED physician and the radiologist as normal. The patient is placed in a sling and discharged to follow up with an orthopedic surgeon. Two days later the orthopod finds the patient has a posterior dislocation The patient notifies the ED. The hospital’s Risk Management Department goes into action.

Plaintiff: My pain and limited ROM was way off the scale compared to a minor sprain. Both the ED doc and the radiologist misread my x-rays. You should have suspected a posterior shoulder dislocation and done a CT scan. Your failure to recognize this caused me more pain, time off, and medical expenses. We need to talk.

Defense: You’re right. We’re sorry. We want to make this right.

Result: The orthopedic surgeon was gracious. The ED physician and radiologist both called the patient and apologized. After discussions with the patient (a forgiving and reasonable gentleman), his attorney, and the hospital risk management department, an agreement was reached to forgive all bills, pay his expenses for relocating the shoulder and therapy, compensate him for time loss from work, plus a small amount for pain, suffering, and inconvenience. The total amount was under $100,000, split between the radiologist, the ED physician, and the hospital. The patient recovered nicely.

Takeaway:

  • Saying you’re sorry helps, along with having a good relationship with your backup docs and risk management department.
  • Posterior shoulder dislocations are uncommon but commonly missed.
  • FOOSH is the typical mechanism, with seizures second.
  • Pain and limited ROM are impressive – as one can imagine. The patient just hurts too much for nothing to be wrong. This alone should trigger the “critical thought”: “Could this be a posterior dislocation?”
  • The shoulder is usually held in adduction and internal rotation.
  • The humeral head on x-ray may be internally rotated and appear as a “lightbulb on a stick,” but it may also be read as normal.
  • High index of suspicion required. A CT will make the diagnosis, especially if one suspects a humeral head fx and finds none..

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http://eorif.com/Shoulderarm/Images/Shoulder-dislocationP1.jpg

References/Further Reading:

  1. Lightbulb on a stick image: http://eorif.com/Shoulderarm/Images/Shoulder-dislocationP1.jpg
  2. Posterior Shoulder Dislocation. Life in the Fastlane (blog). Mike Cadogan http://lifeinthefastlane.com/posterior-shoulder-dislocation/ (includes excellent x-ray images)

“There are no mistakes, save one: the failure to learn from a mistake.” – Robert Fripp

TOXCARD: TOXIC ALCOHOL POISONING

Author: Kristin E. Fontes, MD (Emergency Physician, Santa Barbara Cottage Hospital and Goleta Valley Cottage Hospital) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center)

screen-shot-2017-01-08-at-11-30-27-pm
Case presentation:

A 28-year-old female is brought to the emergency department by ambulance from home after her roommate found her disoriented and poorly responsive. The roommate reports finding a small container of antifreeze in the patient’s bedroom. Vital signs are as follows: T 37.0C, HR 65, BP 126/76, RR 32, and SpO2 98% on room air.  Venous blood gas shows pH 6.97, pCO2 21, pO2 38, HCO3 4.8, and lactate 6.75.

Question:

What are the laboratory abnormalities that can occur with toxic alcohol poisoning and how can it be treated?

Pearl:

Common features of toxic alcohol poisoning are elevated anion gap metabolic acidosis and elevated osmolar gap (the latter being a distinguishing feature from ethanol poisoning); osmolar gap usually elevated early after ingestion.(1,2)

Recall the toxic alcohol metabolites and their effects:

toxic alcohol metabolism

  • EG toxicity can cause significant renal failure due to oxalate crystal deposition in the kidneys and glycolic acid, which is directly nephrotoxic; hypocalcemia and tetany can also result due to oxalate binding to calcium.(1)
  • MeOH toxicity classically causes visual disturbances (“snowfield” vision) due to formic acid-induced optic neuropathy.(1)
  • Isopropanol toxicity causes ketosis without acidosis (no lactic acid formed!).  Usually benign clinical course but can occasionally cause hemorrhagic gastritis. Fomepizole and HD not usually indicated.(1)
  • Propylene glycol toxicity often due to intravenous medication preparations containing this alcohol (e.g., diazepam, lorazepam, esmolol, nitroglycerin, phenobarbital, phenytoin) can result in severe lactic acidosis.(1)
Treatment Approach:
  • Fomepizole competitively inhibits alcohol dehydrogenase, which is involved in the metabolism of all alcohols, including ethanol. It is given to prevent the buildup of toxic metabolites from ethylene glycol (glycolic acid, glyoxylic acid, and oxalic acid) and methanol (formic acid) whose deposition in tissues can cause irreparable damage.(1)
  • Fomepizole is indicated for MeOH or EG ingestion resulting in a metabolic acidosis with an elevated osmolar gap (not accounted for by ethanol) and a serum MeOH or EG level of at least 20 mg/dL.(1)
  • Fomepizole dosing: 1) Load: 15 mg/kg (max 1.5 g) IV, diluted in 100 mL of normal saline or 5% dextrose, infused over 30 minutes; 2) Maintenance: 10 mg/kg IV every 12 hours for 4 doses, then increase to 15 mg/kg until serum toxic alcohol level is less than 20 mg/dL.(1,3)
  • Hemodialysis is indicated for toxic alcohol poisoning with an elevated osmolar gap and/or severe metabolic acidosis refractory to standard therapy, refractory hypotension, or end organ damage (i.e. acute renal failure).(1,3)
  • Vitamin Supplementation: Give folic or folinic acid to patients with MeOH toxicity to divert metabolism away from formic acid to carbon dioxide and water. Give folic acid, pyridoxine, and thiamine to patients with EG toxicity to divert metabolism to nontoxic metabolites.(1,3)
Main points:

Consider toxic alcohol poisoning in a patient with an unexplained elevated anion gap metabolic acidosis and elevated osmolar gap. Consider fomepizole and/or HD in patients with severe toxic alcohol poisoning, especially if refractory to standard therapy.

 

References:
  1. Olson KR & California Poison Control System. (2012). Poisoning & drug overdose. New York: Lange Medical Books/McGraw-Hill.
  2. Emmett M and Palmer BF. Serum osmolal gap. In: UpToDate, Forman JP (Ed), UpToDate, Waltham, MA, 2016.
  3. LeBlanc C, Murphy N. Should I stay or should I go?: toxic alcohol case in the emergency department. Can Fam Physician 2009 Jan;55(1):46-9.

A Lump in the Groin: The Diagnostic Dilemma

Authors: Molly L. Tolins, MD and Sachita Shah, MD (Division of Emergency Medicine, Department of Medicine, University of Washington, Seattle WA) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

The Case: Groin Pain

A 53-year-old male with a history of IV drug use presents to your emergency department with swelling and pain in his right groin. He shoots in his bilateral groins and says his last injection in the right groin was about a week ago; he noticed the swelling and pain over the last few days. He denies fevers, chills, malaise, lower extremity weakness, numbness, or swelling. His vitals are normal, and on your exam he has an indurated mass, approximately 4 cm in diameter, in his right groin just below the inguinal ligament, tender to palpation, with minimal overlying erythema. He also has several track marks in bilateral groin regions. What do you want to do next? Labs? Ultrasound? CT scan? Call a friend? Discharge with PCP follow up?

Groin Mass: The Differential

The differential for a groin mass in someone who injects in their groin is long. Abscess, of course, is high on the differential. However, not all hoof beats are horses, and before you go incising that mass, you have to consider alternatives. These include entities such as retained foreign bodies (broken needle tips), reactive adenopathy, suppurative lymphadenitis, DVT, superficial thrombophlebitis, cellulitis, and femoral artery pseudoaneurysm.

These diagnoses require very different management, and so differentiating them is critical. Luckily, bedside ultrasound is the quickest and best modality for assessment in most cases. In this patient’s case, you decide to do a quick bedside ultrasound, and find this:

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Figure 1. Bedside ultrasound, 2-dimensional gray scale, with the common femoral artery on the left of the screen in cross-section, demonstrating a large fluid-filled mass.

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Figure 2. Same view bedside ultrasound, with color Doppler applied, demonstrating bidirectional flow within the mass.

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Figure 3. Pulsed wave Doppler overlying the neck of the mass on bedside ultrasound showing pulsatile flow.

Diagnosis

This patient has an infected right common femoral artery (CFA) pseudoaneurysm. CTA confirms the bedside ultrasound findings (Fig. 4).

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Figure 4. CTA Pelvis with new right CFA irregular pseudoaneurysm measuring 4.3 x 2.2 cm. There is soft tissue attenuation stranding around the aneurysm sac suggesting infection/mycotic aneurysm.

Pathophysiology

Traumatic arterial injury is the most common cause of pseudoaneurysms. Infected femoral artery pseudoaneurysm is one of the most common arterial complications of repeated non-sterile punctures in injection drug users. 1  Femoral pseudoaneurysms are also reported to occur in 1% of diagnostic arterio-grams and up to 8% of therapeutic endovascular interventions.2

Presentation

Pseudoaneurysms follow arterial damage, allowing blood to escape into surrounding tissue, with a fibrin wall gradually forming, resulting in a false aneurysm.3,4  The natural history of a pseudoaneurysm is to grow gradually over time; an abrupt increase in size should raise concern for a ruptured aneurysm.

Most patients present with masses and can have leg swelling or limitation of activity of their leg. Some patients with a ruptured pseudoaneurysm will present with active bleeding. A femoral pseudoaneurysm can masquerade as an abscess, as both often present with groin pain and swelling, and not all pseudoaneurysms will be pulsatile.2 Mistaking the two can be catastrophic.

Work Up

The diagnosis of a pseudoaneurysm may be confirmed with color Doppler ultrasonography, computed tomography, or angiography.There are 3 classic signs of a pseudoaneurysm in sonography: a communication between the artery and the pseudoaneurysm (Fig.1); a yin-yang sign, which indicates bidirectional flow because of the swirling of blood within the pseudoaneurysm cavity (Fig. 2); and a “to-and-fro” on pulsed wave doppler within the neck, indicating reversal of flow in the neck during diastole (Fig. 3).  Bedside ultrasonography has a sensitivity and specificity of 94% and 94%-97%, respectively in the evaluation of possible vascular injury causing pseudoaneurysm,6 and should be performed prior to consideration of incision and drainage of what might otherwise appear to be an abscess.

Computed tomography angiography (CTA) is also a valuable diagnostic tool, allowing assessment of the pseudoaneurysm, surrounding structures, arterial inflow, and distal run-off of the leg.6   This can be especially helpful when an infected pseudoaneurysm is suspected, and for surgical planning.

Management/Disposition

Approach to the management of a pseudoaneurysm depends on its anatomical location. Potential treatment modalities include radiological management, including ultrasound guided compression repair (UGCR); endovascular management, with the usage of embolization, perfusion balloons, and placement of covered stents/endoluminal prostheses; and open surgical management with ligation.2

Infected femoral artery pseudoaneurysms in IV drug users should not be managed expectantly. The mass will inevitably grow and rupture, and thus surgical therapy and vascular consultation should be pursued as soon as possible. If grafts are placed, these patients are at higher risk for infection of their grafts and need of a second surgery for graft removal.6

When there is evidence that the femoral pseudoaneurysm is ruptured, such as active bleeding or rapid expansion, emergent surgery is the cornerstone of treatment.Hemodynamic support with product resuscitation and vasopressors may be necessary until definitive treatment can be provided. Active external bleeding from the site should be stopped with direct pressure and/or packing.8

In all cases of infected femoral artery pseudoaneurysms, there is a high risk of infection both pre- and post-operatively. Thus, all patients with a suspected infected CFA pseudoaneurysm should be covered with broad-spectrum antibiotics.9

Summary

  • Consider pseudoaneurysm in your differential for groin, axilla, and other lumps before proceeding down an abscess treatment algorithm
  • Your physical exam will not always give you the diagnosis
  • Bedside ultrasonography has a sensitivity and specificity of 94% and 94%-97%, respectively, in the evaluation of pseudoaneurysm
  • Femoral artery pseudoaneurysm requires surgical consultation, and surgical management is the mainstay of treatment
  • Administer broad spectrum antibiotics in septic patients or those with evidence of infected pseudoaneurysm

 

References / Further Reading

  1. Qiu, W. Zhou, W. Zhou, X. Tang, Q. Yuan, X. Zhu, Y. Yang, J. Xiong. The Treatment of Infected Femoral Artery Pseudoaneurysms Secondary to Drug Abuse: 11 Years of Experience at a Single Institution. Annals of Vascular Surgery, 2016; 36: 35–43
  2. Petrou, I. Malakos, S. Kampanarou, N. Doulas, V. Voudris. Life-threatening rupture of a femoral pseudoaneurysm after cardiac catheterization. Open Cardiovasc Med J. 2016; 10: 201-204.
  3. Gudena, N. Khetan. Swelling of volar aspect of the wrist. Postgrad Med J, 81 (2005) e9, e11
  4. L. Zitsman. Pseudoaneurysm after penetrating trauma in children and adolescents. J Pediatr Surg, 33 (1998), pp. 1574–1577
  5. Goksu, E., Yuruktumen, A., and Kaya, H. Traumatic pseudoaneurysm and arteriovenous fistula detected by bedside ultrasound. J Emerg Med. 2014; 46: 667–669
  6. Gullo, J., Singletary, E.M., and Larese, S. Emergency bedside sonographic diagnosis of subclavian artery pseudoaneurysm with brachial plexopathy after clavicle fracture. Ann Emerg Med. 2013; 61: 204–206
  7. Etemad-Rezai R., Peck D.J. Ultrasound-guided thrombin injection of femoral artery pseudoaneurysms. Can. Assoc. Radiol. J. 2003;54(2):118–120.
  8. Li Q., Shu C., Jiang X., Li M., Li X., He H. Surgical management of infected pseudoaneurysms of femoral artery caused by narcotics injection.Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2009;34(6):476–480
  9. Salimi J, Shojaeefar A, Khashayar P. Management of infected femoral pseudoaneurysms in intravenous drug abusers: a review of 57 cases.Archives of Medical Research. 2008;39(1):120–124.

The Utility of MRI in the Emergency Department

Author: Adrianna Long, MD (Emergency Medicine Staff at Winn Army Community Hospital, Fort Belvoir, GA) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

It is important that providers make the correct choice for imaging when dealing with emergent conditions. MRI is a costly choice, but sometimes the most appropriate to evaluate for specific pathology. It is imperative to weigh the risk and benefits of MRI as compared to other imaging modalities. Also, in many facilities, MRI is only available during business hours, which makes obtaining emergent MRIs very difficult. So, when is ordering an MRI in the Emergency Department indicated?

MRI of the Brain

MRI has a significantly greater detection rate for acute ischemic infarction than CT, particularly in an early setting.  CT has been reported to have a sensitivity ranging from 73-88% for acute stroke within the first 12 hours. In comparison, MRI has a sensitivity of 93-100% and may be able to detect acute ischemic injury within a few minutes of onset.1,2 However, not all patients that have acute strokes are candidates for interventions including tPA or endovascular therapy, so it is important to choose the appropriate imaging modality as an MRI may not be indicated emergently.

There is no standard imaging protocol for the evaluation of acute stroke or TIA beyond head CT noncontrast. The goal of neuroimaging is to provide rapid information and increase providers’ decision-making with regards to reperfusion therapy without causing harm from delays.3

A study recently published reviewed the imaging of 8,247 patients who were evaluated with TIA or minor stroke in 2011, revealing that approximately 50% of patients underwent MRI imaging within 2 days of presentation. The use of MRI to evaluate TIA or stroke is limited in many facilities with lack of availability, and MRIs are often ordered by inpatient services rather than emergently.4

The American College of Neuroradiology, the American College of Radiology, and Society of NeuroInterventional Surgery have made a joint statement with regards to the imaging of acute stroke and TIA. When determining whether endovascular therapy should be considered, they have found that noncontrast CT with digital subtraction angiography, noncontrast CT with CTA, and MRI with MRA are equivalent options for clinicians.5 Of those imaging modalities, noncontrast CT with CTA is the preferred strategy currently when selecting intraarterial thrombectomy candidates, as CT is widely available and faster.6

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While a cavernous venous thrombosis (CVT) is a rare diagnosis, the use of MRV offers an alternative diagnostic modality. The MRV is more sensitive at diagnosis of a CVT than an unenhanced CT.7 Therefore, when considering CVT as a diagnosis, MRV may be considered for imaging, but CT venography is rapid, readily available, and an accurate technique to detect CVT.7

MRI of the Spine

The early diagnosis of an epidural abscess is essential to minimize patient morbidity and mortality. A study of 63 patients with spinal epidural abscess indicated that a delay in diagnosis greater than 24 hours occurred in 75% of cases, and persistent motor weakness resulted in 45% with diagnostic delays.8 The ACR ranks MRI of the spine with and without contrast as the most appropriate study to evaluate for infectious processes of the spine. When there is clinical suspicion for an epidural abscess, the emergency physician should insist on early MRI to prevent poor neurologic outcomes.9

The sudden onset of neurologic deficit due to neoplasm is another emergency that requires immediate imaging, neurosurgical consult, and treatment with high dose steroids.10

Epidural hematoma is a rare cause of back pain that may be associated with myelopathy and usually the result of recent spinal procedures or trauma. The symptoms may present similarly to an acute disc herniation. Patients who may be of particular risk are those on anticoagulant therapy.10

Cauda equina syndrome (CES) is suspected when there is severe lower back pain and radicular symptoms, especially at L5/S1, with saddle anesthesia and bowel/bladder/sexual dysfunction. The diagnosis of CES requires an emergent MRI followed by rapid surgical decompression.11

Basically, if serious underlying pathology is plausible or there is evidence of neurologic involvement in patients with back pain, MRI is the study of choice.9

MRI to evaluate for appendicitis

 Pediatric patients:

Efforts are being made to decrease ionizing radiation exposure in pediatric patients, and MRI has been shown to be useful for the diagnosis of acute appendicitis.12 MRI protocols have been created with combined use of ultrasound to diagnose appendicitis in many hospitals for adult and pediatric patients. In one institution over 30 months, MRI has been shown to have a sensitivity of 96.8%, specificity of 97.4%, negative predictive value of 98.9%, and positive predictive value of 92.4%.13

A retrospective study at another institution with utilization of MRI for 49 pediatric patients with suspected appendicitis after having indeterminate ultrasound found a sensitivity of 94% and a specificity of 100% for diagnosis of acute appendicitis. There were a total of 16 patients diagnosed with appendicitis. The use of MRI aided clinicians in obtaining final diagnoses as well, including other diagnoses such as pyelonephritis, constipation, pelvic inflammatory disease, ruptured ovarian cyst, hemorrhagic cyst, and epiploic appendagitis.14

A study of 662 pediatric patients imaged with CT versus MRI found  no significant difference in time to antibiotic administration, time to appendectomy, perforation rate, or hospital length of stay for patients imaged with either modality.15

Pregnant patients:

In 2011, the American College of Radiology (ACR) designated ultrasound as the initial imaging study choice to evaluate for acute appendicitis in pregnant patients.16 However, there have been multiple studies published indicating that ultrasound may not be the most appropriate imaging study to evaluate for appendicitis in pregnant patients since nonvisualization of the appendix has been reported to range as high as 68-97%.17-19 The efficiency of ultrasound may be limited due to bowel gas, body habitus, and anatomic displacement of the appendix, as well as patient tolerance in the setting of an acute abdomen.18

A meta-analysis of 6 articles analyzing the diagnostic strength of MRI in 359 pregnant women with suspected appendicitis found a specificity of 98% and 99% negative predictive value when a normal appendix is visualized.20

The ACR endorses the use of MRI when ultrasound cannot provide diagnostic information in pregnant patients. MRI has been shown to be useful for multiple diagnoses in pregnant patients with acute abdominal/pelvic pain.21 A retrospective study including 171 patients undergoing MRI with a pregnant appendicitis protocol had an appendix visualization rate of 69%. Furthermore, the overall diagnostic rate was 43.3% finding ovarian masses, ovarian torsion, uterine fibroid tumors, ectopic pregnancies, hernias, renal abscess, as well as appendicitis.22

MRI of the Hip

The use of MRI in the Emergency Department to evaluate for suspected hip fracture can be useful when the clinician has a high suspicion and there is a negative Xray or CT. Despite the use of CT to evaluate for hip fractures, there are still 2-4% with missed hip fractures.23,24 While there is a general consensus that a delay to surgery >48 hours is associated with a higher mortality, and a retrospective study of 6,638 patients with hip fractures indicated that surgery before 12 hours improved survival.25 The results of this study suggest that rapid diagnosis of a hip fracture is essential so patients can receive the appropriate treatment as soon as possible to avoid complications.

There is 100% sensitivity and 99% specificity in detecting hip fractures with abbreviated MRI. This hip protocol MRI may also be used to detect avascular necrosis (AVN) with a sensitivity of 97% and 100% specificity.26

Hazards in MRI scanning

Patients should be adequately screened prior to obtaining MRI, and alternative imaging should be considered in patients with:

  1. Renal disease (especially a GFR lower than 30mL/min)
  2. Allergy to gadolinium
  3. History of injury involving projectiles
  4. History of surgery with retained metallic items, e.g. surgical clips, pacemaker, stents
  5. Claustrophobia27

Nephrogenic systemic fibrosis (NSF) is a potentially fatal condition that has been associated with the use of gadolinium.28 A study of 8997 patients who received gadolinium showed a total of 15 patients (0.17%) who subsequently developed NSF, with a GFR of less than 30mL/min in all of the affected patients.29

Of note, there is inherent risk in sending patients who may become unstable during transport and time to obtain the MRI. Most MRIs require time away from the ED, utilizing emergency staff and equipment outside of the ED, for a prolonged period, or there may be a need to transport to a facility where MRIs are available.

Bottom line:

An MRI should only be ordered in the ED when the patient’s treatment and/or management will be affected.

The misuse of MRIs in the ED generates unnecessary costs to patients and increased time in the department.  It is essential to weigh the risk(s) of ordering an MRI for your patient in the ED.

The indications for emergency MRI Brain include clinical concern for acute ischemic stroke, particularly wherein the management may differ with possible intervention versus less aggressive treatment plans.

If there is clinical concern for new spinal cord compression from disease or injury, an emergency MRI evaluation is necessary. 

The indications for emergency spinal MRI include suspicion for:

  • Spinal cord compression (herniated disc, burst fracture, tumors, etc)
  • Spinal infection (i.e. abscess)
  • Spinal trauma (epidural hemorrhage, etc)
  • Demyelination with acute neurologic changes

Additionally, emergency MRIs may be considered if there is concern for:

  • Appendicitis in the pregnant or pediatric patient
  • Hip fracture not detected on plain film or CT

 

References/Further Reading:

  1. Krieger DA, Dehkharghani S. Magnetic Resonance Imaging in Ischemic Stroke and Cerebral Venous Thrombosis. Top Magn Reson Imaging. 2015;24(6):331-352.
  2. Lev MH. CT versus MR for acute stroke imaging: is the “obvious” choice necessarily the correct one? AJNR Am J Neuroradiol. 2003;24(10):1930-1931.
  3. Lin MP, Liebeskind DS. Imaging of Ischemic Stroke. Continuum (Minneap Minn). 2016;22(5, Neuroimaging):1399-1423.
  4. Chaturvedi S, Ofner S, Baye F, et al. Have clinicians adopted the use of brain MRI for patients with TIA and minor stroke? Neurology. 2017;88(3):237-244.
  5. Wintermark M, Sanelli PC, Albers GW, et al. Imaging recommendations for acute stroke and transient ischemic attack patients: a joint statement by the American Society of Neuroradiology, the American College of Radiology and the Society of NeuroInterventional Surgery. J Am Coll Radiol. 2013;10(11):828-832.
  6. Goyal M, Hill MD, Saver JL, Fisher M. Challenges and Opportunities of Endovascular Stroke Therapy. Ann Neurol. 2016;79(1):11-17.
  7. Leach JL, Fortuna RB, Jones BV, Gaskill-Shipley MF. Imaging of cerebral venous thrombosis: current techniques, spectrum of findings, and diagnostic pitfalls. Radiographics. 2006;26 Suppl 1:S19-41; discussion S42-13.
  8. Davis DP, Wold RM, Patel RJ, et al. The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. J Emerg Med. 2004;26(3):285-291.
  9. Seidenwurm DJ, Wippold FJ, 2nd, Cornelius RS, et al. ACR Appropriateness Criteria((R)) myelopathy. J Am Coll Radiol. 2012;9(5):315-324.
  10. Arce D, Sass P, Abul-Khoudoud H. Recognizing spinal cord emergencies. Am Fam Physician. 2001;64(4):631-638.
  11. Mukherjee S, Thakur B, Crocker M. Cauda equina syndrome: a clinical review for the frontline clinician. Br J Hosp Med (Lond). 2013;74(8):460-464.
  12. Moore MM, Brian JM, Methratta ST, et al. MRI for clinically suspected pediatric appendicitis: case interpretation. Pediatr Radiol. 2014;44(5):605-612.
  13. Kulaylat AN, Moore MM, Engbrecht BW, et al. An implemented MRI program to eliminate radiation from the evaluation of pediatric appendicitis. J Pediatr Surg. 2015;50(8):1359-1363.
  14. Rosines LA, Chow DS, Lampl BS, et al. Value of gadolinium-enhanced MRI in detection of acute appendicitis in children and adolescents. AJR Am J Roentgenol. 2014;203(5):W543-548.
  15. Aspelund G, Fingeret A, Gross E, et al. Ultrasonography/MRI versus CT for diagnosing appendicitis. Pediatrics. 2014;133(4):586-593.
  16. Rosen MP, Ding A, Blake MA, et al. ACR Appropriateness Criteria(R) right lower quadrant pain–suspected appendicitis. J Am Coll Radiol. 2011;8(11):749-755.
  17. Israel GM, Malguria N, McCarthy S, Copel J, Weinreb J. MRI vs. ultrasound for suspected appendicitis during pregnancy. J Magn Reson Imaging. 2008;28(2):428-433.
  18. Lehnert BE, Gross JA, Linnau KF, Moshiri M. Utility of ultrasound for evaluating the appendix during the second and third trimester of pregnancy. Emerg Radiol. 2012;19(4):293-299.
  19. Vu L, Ambrose D, Vos P, Tiwari P, Rosengarten M, Wiseman S. Evaluation of MRI for the diagnosis of appendicitis during pregnancy when ultrasound is inconclusive. J Surg Res. 2009;156(1):145-149.
  20. Long SS, Long C, Lai H, Macura KJ. Imaging strategies for right lower quadrant pain in pregnancy. AJR Am J Roentgenol. 2011;196(1):4-12.
  21. Furey EA, Bailey AA, Pedrosa I. Magnetic resonance imaging of acute abdominal and pelvic pain in pregnancy. Top Magn Reson Imaging. 2014;23(4):225-242.
  22. Theilen LH, Mellnick VM, Longman RE, et al. Utility of magnetic resonance imaging for suspected appendicitis in pregnant women. Am J Obstet Gynecol. 2015;212(3):345 e341-346.
  23. Hakkarinen DK, Banh KV, Hendey GW. Magnetic resonance imaging identifies occult hip fractures missed by 64-slice computed tomography. J Emerg Med. 2012;43(2):303-307.
  24. Iwata T, Nozawa S, Dohjima T, et al. The value of T1-weighted coronal MRI scans in diagnosing occult fracture of the hip. J Bone Joint Surg Br. 2012;94(7):969-973.
  25. Bretherton CP, Parker MJ. Early surgery for patients with a fracture of the hip decreases 30-day mortality. Bone Joint J. 2015;97-B(1):104-108.
  26. Khurana B, Okanobo H, Ossiani M, Ledbetter S, Al Dulaimy K, Sodickson A. Abbreviated MRI for patients presenting to the emergency department with hip pain. AJR Am J Roentgenol. 2012;198(6):W581-588.
  27. Institute for Magnetic Resonance Safety E, and Research (IMRSER). Magnetic Resonance (MR) Procedure Screening Form For Patients and Magnetic Resonance (MR) Environment Screening Form for Individuals. 2017.
  28. Grobner T. Gadolinium–a specific trigger for the development of nephrogenic fibrosing dermopathy and nephrogenic systemic fibrosis? Nephrol Dial Transplant. 2006;21(4):1104-1108.
  29. Prince MR, Zhang H, Morris M, et al. Incidence of nephrogenic systemic fibrosis at two large medical centers. Radiology. 2008;248(3):807-816.

 

Croup: ED-focused Highlights

Authors: James Costakis, MD (EM Resident Physician, UW/Harborview, Seattle, WA), Siobhan Thomas-Smith, MD (Pediatrics Resident Physician, Seattle Children’s Hospital, Seattle, WA), and Rebekah Burns, MD (Pediatric Emergency Attending Physician, Seattle Children’s Hospital, Seattle, WA) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

Case 1

A 2-year-old boy presents with sudden onset of cough and difficulty breathing that woke him from sleep. Parents thought his breathing was labored and brought him to the ED. He has a history of reactive airway disease but has never been hospitalized.

Vitals in the ED:

Temperature 100F, heart rate 110, blood pressure 90/60, respiratory rate 30, oxygen saturation 98% on room air.

Exam is remarkable for a fatigued boy who refuses to speak. He has stridor at rest, tracheal tug, and moderate intercostal retractions. You do not appreciate wheezing on exam. He has a mild scattered erythematous rash on his chest and arms.

 

Case 2

A 10-year-old boy presents with fever and vomiting. Parents report two days of fever up to 104F, associated with myalgias, nausea, and mild cough. Vomiting was prominent today, and parents are worried that he is dehydrated. For the past day, his voice has become slightly hoarse, and his breathing audible.

Vitals in the ED:

Temperature 103F, heart rate 120, blood pressure 110/70, respiratory rate 26, oxygen saturation 91% on room air.

Exam is remarkable for suprasternal and supraclavicular retractions, as well as audible stridor at rest.

 

Physiology of Croup

Croup is a spectrum of illness characterized by varying degrees of inflammation in the upper respiratory tract, with possible involvement of the lower respiratory tract. Patients may have laryngotracheitis, laryngotracheobronchitis, or laryngotracheobronchopneumonitis. In 75% of cases, parainfluenza virus is responsible [6]. Otherwise, RSV, metapneumovirus, influenza, adenovirus, coronavirus, or even mycoplasma can cause a similar syndrome [6,8]. Some patients have recurrent bouts of upper airway edema causing a croup-like syndrome, which is referred to as spasmodic croup. This is thought to be potentially related to hypersensitivity to viral antigens.

 

Classic presentation

Croup primarily affects children from 6 months to 3 years of age, with a peak incidence of 5% per year in 2-year-olds [8]. Boys are 1.4 times more likely than girls to develop croup [8]. Typically, it occurs in the late fall or early winter [8]. Patients may or may not complain of a short prodromal upper respiratory infection. The acute phase of illness is characterized by stridor, barky cough, hoarseness, and sometimes fever. Symptoms often come on abruptly at night. Within 48 hours, most patients have recovered, but they may have lingering upper respiratory symptoms for about a week [4,9].

 

Diagnosis of Croup

Croup is diagnosed clinically. Chest X-ray and respiratory viral panel are sometimes used when one is considering an alternative diagnosis, but otherwise do not meaningfully affect the patient’s clinical course and are not recommended in uncomplicated croup [12].

The differential diagnosis of croup includes other causes of upper airway obstruction, gastroesophageal reflux, and allergic syndromes such as angioedema or spasmodic croup.

Other causes of upper airway obstruction include:

  • Bacterial tracheitis
  • Laryngomalacia
  • Tracheomalacia
  • Vascular rings
  • Epiglottitis (unlikely if vaccinated)
  • Foreign body aspiration
  • Peritonsillar abscess
  • Retropharyngeal abscess
  • Tracheo-esophageal fistula

A high index of suspicion for these alternative diagnoses is critical, particularly in patients who are presumptively diagnosed with croup but fail to follow the expected clinical course. Some red flags include:

  • Failure to respond to racemic epinephrine after 30 minutes
  • Trouble handling secretions
  • Oxygen requirement
  • Wheezing

 

How to Identify Sick Patients

Croup is common, accounting for 15% of ED visits by children with respiratory complaints and for 5% of ED admissions in children under 6 years of age [4,5]. Luckily, croup is usually a mild syndrome requiring minimal intervention – about 85% of children presenting to the ED have mild croup [10]. Only 1 to 3% of children with croup are intubated, and even then the mortality rate of children intubated for croup is only 0.5% [4]. Even so, early identification and aggressive treatment are critical in this subgroup of very sick children in order to maintain this low mortality rate.

How can we quickly identify patients who are in more severe respiratory distress? The Westley croup score has been around since the 1970’s and might help predict which patients need racemic epinephrine [3]. The score stratifies patients based on level of consciousness, cyanosis, stridor, air entry, and retractions. However, the score is typically used in research studies to quantify the efficacy of an intervention, and it has not been prospectively validated to predict mortality, intubation, or hospital admission.

At Seattle Children’s Hospital, a child is considered to have “severe” croup when they have stridor at rest, plus one of the following [17]:

  • Moderate intercostal retractions
  • Tachypnea
  • Agitation or restlessness
  • Fatigue
  • Difficulty speaking or feeding

These patients warrant racemic epinephrine, as discussed below. Notably, decreasing stridor can be an ominous sign, just as decreasing wheezing can suggest impending respiratory failure in asthmatics. Be on the lookout for lethargy, increasing fatigue, and worsening mental status. In the lethargic patient with decreasing stridor, decreased level of alertness, and hypoxemia, intubation may be required.

 

Treatment

Historically, cool mist or humidified air was used to treat croup, but they are no longer recommended as studies have consistently failed to show clinical improvement with these interventions [13-15]. The primary adjuncts to support of airway, breathing, and circulation are dexamethasone and racemic epinephrine.

Dexamethasone has been found to improve the Westley score at 6 and 12 hours (but not at 24 hours), with a NNT of 5 to improve the score [2]. Patients typically require less epinephrine, spend less time in the ED or hospital (by about 12 hours), and have fewer return visits or readmissions (RR of return or readmission 0.5) when treated early with dexamethasone [2].

The dose of dexamethasone is 0.6 mg/kg, rounded to the nearest 2mg, up to a maximum dose of 16mg. Lower doses may be as effective, but some studies have seen more patients improved at 12 hours with the higher dose [16]. At Seattle Children’s Hospital, all children with croup of any severity receive dexamethasone. Repeat doses are rarely given [17].

Racemic epinephrine may help by causing mucosal vasoconstriction and decrease subglottic edema. It has been found to improve symptoms at 30 minutes, but the effect is normally gone by 2 hours [1].

The dose of racemic epinephrine is 0.5 mL of nebulized 2.25% solution, diluted in 3 mL of normal saline. At Seattle Children’s, this is given as soon as possible to children with “severe” croup, and can be re-dosed every 2 hours up to 3 times [17]. Further doses are typically given as an inpatient, and failure to improve after 3 doses suggests a possible alternative or concomitant diagnosis. This medication is most commonly given to those with stridor at rest.

There is conflicting data on whether heliox can be beneficial in croup. Most studies assessing heliox have looked at children with moderate to severe croup [18]. Heliox may improve the croup score, even compared to racemic epinephrine, starting at 90 minutes and lasting up to 4 hours, but no difference was found after 4 hours [18]. Overall, the data are conflicting, and at this point it is impossible to make a strong recommendation on administration of heliox. Currently, it may be considered as an adjunct therapy in a patient with severe croup with only partial response to racemic epinephrine.

 

Disposition

Patients may have stridor with activity and still do well at home. However, stridor at rest warrants further intervention. Children should be able to talk and feed with minimal retractions. At Seattle Children’s, patients must be on room air and must not have received racemic epinephrine in the 2 hours prior to discharge [17].

Patients not meeting discharge criteria within 2 hours of dexamethasone are likely to require admission. Respiratory distress despite multiple doses of racemic epinephrine suggests likely need for ICU care and consideration of ENT consultation for direct laryngoscopy.

 

Case Resolution

Case 1

This patient may have classic laryngotracheitis from parainfluenza. The viral exanthem is non-specific. However, if you are concerned about anaphylaxis, it would not be wrong to administer intramuscular epinephrine. Otherwise, his stridor at rest and moderate intercostal retractions warrant racemic epinephrine in addition to dexamethasone.

Case 2

This patient is older than most patients with classic croup. Given his fever, age, and poor oxygenation, he requires consideration of a broad differential. Chest X-ray and viral panel are reasonable. He may have influenza causing a croup-like syndrome with stridor and respiratory distress, and may benefit from racemic epinephrine to decrease upper airway inflammation.

 

Pearls & Takeaways

  • Do not routinely obtain chest X-ray or respiratory viral panel in children with uncomplicated croup.
  • In patients who fail to respond to racemic epinephrine, or who are in significant respiratory distress, the differential must be initially very broad, with particular concern for bacterial tracheitis.
  • All patients with croup of any severity can benefit from dexamethasone.
  • Racemic epinephrine can help for a short time, and if it doesn’t, broaden your differential.

 

References / Further Reading

  1. Bjornson C, Russell K, Vandermeer B, Klassen TP, Johnson DW. Nebulized epinephrine for croup in children. Cochrane Database of Systematic Reviews 2013, Issue 10. Art. No.: CD006619.
  2. Russell KF, Liang Y, O’Gorman K, Johnson DW, Klassen TP. Glucocorticoids for croup. Cochrane Database of Systematic Reviews 2011, Issue 1. Art. No.: CD001955.
  3. Westley CR, Cotton EK, Brooks JG. Nebulized racemic epinephrine by IPPB for the treatment of croup: a double-blind study. Am J Dis Child. 1978 May;132(5):484-7.
  4. Johnson DW. Croup. BMJ Clin Evid. 2009; 2009: 0321.
  5. Cherry JD. Clinical practice. Croup. N Engl J Med. 2008;358(4):384–391.
  6. Rihkanen H, Rönkkö E, Nieminen T, et al. Respiratory viruses in laryngeal croup of young children [published correction appears in J Pediatr. 2008;153(1):151]. J Pediatr. 2008;152(5):661–665.
  7. Mazza D, Wilkinson F, Turner T, Harris C. Evidence based guideline for the management of croup. Aust Fam Physician. 2008 Jun;37(6 Spec No):14-20.
  8. Denny FW, Murphy TF, Clyde WA Jr, Collier AM, Henderson FW. Croup: an 11-year study in a pediatric practice. Pediatrics. 1983;71(6):871–876.
  9. Bjornson CL, Johnson DW. Croup. 2008;371(9609):329–339.
  10. Bjornson CL, Johnson DW. Croup-treatment update. Pediatr Emerg Care. 2005;21(12):863–870.
  11. Chan A, Langley J, Leblanc J. Interobserver variability of croup scoring in clinical practice. Paediatr Child Health. 2001;6(6):347–351.
  12. Swingler GH, Zwarenstein M. Chest radiograph in acute respiratory infections. Cochrane Database Syst Rev. 2008;(1):CD001268.
  13. Scolnik D, Coates AL, Stephens D, Da Silva Z, Lavine E, Schuh S. Controlled delivery of high vs low humidity vs mist therapy for croup in emergency departments. JAMA. 2006;295(11):1274–1280.
  14. Moore M, Little P. Humidified air inhalation for treating croup. Cochrane Database Syst Rev. 2010;(9):CD002870.
  15. Moore M, Little P. Humidified air inhalation for treating croup. Fam Pract. 2007;24(4):295–301.
  16. Kairys SW, Olmstead EM, O’Connor GT. Steroid treatment of laryngotracheitis: a meta-analysis of the evidence from randomized trials. Pediatrics. 1989;83(5):683–693.
  17. seattlechildrens.org/pdf/croup-pathway.pdf
  18. Moraa I, Sturman N, McGuire T, van Driel ML. Cochrane Database Syst Rev. 2013 Dec 7;(12):CD006822.

ToxCard: TCA Poisoning

Author: Tharwat El Zahran, MD (Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center) screen-shot-2017-01-08-at-11-30-27-pm
Case Presentation:

2 yo male child presented to the ED with status epilepticus. His parents found an empty bottle of amitriptyline at home. He was intubated, given benzodiazepines and antiepileptic drugs. VS: BP 70/30, T 106 F, RR 24, HR 98, sat 98% RA, glucose 100 mg/dl. EKG is shown below.

EKG TCA PED

Question

What EKG findings occur in tricyclic antidepressant (TCA) poisoning? And how are they treated?

Pearl

TCAs alter the conformation of the sodium channel and slow the rate of rise of the action potential, which produces both negative dromotropic and inotropic effects. Sodium bicarb is the primary treatment for TCA poisoning.

  • All TCA are competitive antagonists of the muscarinic acetylcholine receptors and antagonize peripheral α1 adrenergic receptors.
  • Most prominent effects of TCA overdose result from binding to cardiac Na channels.
  • Acute ingestion 10-20 mg/kg of most TCAs cause cardiovascular and CNS toxicity. In children,  >5mg/kg results in toxicity.(1)
  • Signs of acute cardiovascular toxicity are refractory hypotension, acidosis, and arrhythmias. EKG indicators include intraventricular conduction delay (R shift of QRS axis and prolonged QRS), R in avR≥ 3mm, R/S>0.7 and arrhythmias. A QRS≥100 msec indicates increased incidence of serious toxicity, including coma, intubation, hypotension, seizures, and dysrhythmias. Sinus tachycardia is the most common EKG abnormality. (2)(3)
  • Acute neurological toxicity include AMS, delirium, agitation , seizures, and/or psychotic behavior with hallucinations, lethargy, coma.
Treatment approach
  • If the decision is made to intubate, avoid apnea, consider awake intubation, pretreat w benzos to raise seizure threshold and hyperventilate to promote alkalosis.(4)
  • If the EKG indicates signs of TCA poisoning as mentioned above,  give 1-2 meq/kg of sodium bicarb IV boluses at 3-5 min intervals.(4)
  • Continue bicarb drip until QRS duration <100, vitals stable, Na ~150, pH ~7.55. Watch for hypokalemia and hypocalcemia with bicarb drip.  Consider hypertonic saline (3%) if refractory or if serum pH>7.55.(4)
  • Hypotension unresponsive to sodium bicarb, or fluid boluses should be treated with vasopressors (norepi recommended).(4)
  • Treat dysrhythmias with lidocaine bolus of 1mg/kg IV followed by infusion of 20-50 mcg/kg/min.
  • Benzodiazepines, barbiturates, or propofol are recommended for seizures. Consider continuous EEG monitoring with neuromuscular blockade in refractory cases. Avoid phenytoin.(4)
  • For refractory cardiovascular poisoning consider intralipid or ECMO if available.(4)
Main point

TCAs are sodium channel blockers and primary treatment of TCA poisoning is sodium bicarb. The EKG abnormalities like QRS≥100,  R wave in avR ≥3mm, and R/S> 0.7 can predict significant toxicity.  Sodium bicarb displaces the TCA from the Na binding site by raising the Na+ gradient and increasing the pH.  Prolonged resuscitation might be necessary.

References
  1. Caksen et al. Acute amitriptyline intoxication: an analysis of 44 children. Human & Experimental Toxicology (2006) 25: 107-110
  2. Olgun et al. Clinical, Electrocardiographic, and Laboratory Findings in Children With Amitriptyline Intoxication. Pediatr Emer Care 2009;25: 170-173
  3. Paksu et al. Amitriptyline overdose in emergency department of university hospital: Evaluation of 250 patients. Human and Experimental Toxicology 2014;33:980–990
  4. Goldfrank’s Toxicologic Emergencies, 10th E, Chapter 71: Cyclic Antidepressants, p 972- 982.

 

 

Contrast-Induced Nephropathy: Confounding Causation

Author: Richard Sinert, DO (Professor of Emergency Medicine / Vice Chair of Research, SUNY Downstate Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

I would like to applaud the study “Risk of Acute Kidney Injury After Intravenous Contrast Media Administration” by Hinson et al[1] in the February 2017 issue of Annals of Emergency Medicine.  Before discussing the details of this study, I would like to give a historical perspective on how the study of CIN has evolved.

Since the first observation by Bartels et al[2] of the association between between contrast administration and Acute Kidney Injury (AKI), multiple studies gave further added weight to the association between intravenous contrast and AKI[3-7].

Although CIN is defined by a relatively small change in serum creatinine (SCr) (25% from baseline or an absolute increase of 0.5 mg/dl 48-72 hours post infusion), the consequences for CIN patients at least on the surface seemed dire.  Among cardiac catheterization patients, CIN increased the mortality rates[3] from 6% to 16% in one study[7] and from 0.6% to 31% in another[6].  Higher composite mortality rates and need for renal replacement (relative risk = 36) were also observed in patients who met the definition for CIN following CT-PA, after intravenous contrast in pulmonary embolism patients who developed CIN[4].

At this point an iatrogenic injury (CIN) was linked to an easily measured disease marker (timed changes in SCr) that seemed to be associated with adverse outcomes.  Not surprisingly, the medical community with the best of intentions studied the risks[5],[6] and a wide-range[7],[8],[9] of potential measures to prevent CIN.

Yet all these studies documenting CIN incidence, risks, outcomes, and prophylactic strategies suffer a bias common to many observational studies— confounding bias[10],[11].   Confounding bias occurs when an exposure is inappropriately causally linked to an outcome, when a separate exposure (confounding variable) other than the one of interest better explains the observed outcome.  Since the definition of CIN requires a second timed measurement of SCr, these studies must select for a relatively ill group of hospitalized patients undergoing repeated laboratory testing; selection bias must be considered.  Decrements in kidney function signaled by a rise of SCr could have occurred from the incident disease before or after contrast administration.  In addition, intercurrent hemodynamic instability (eg., sepsis, hemorrhage, diuresis) and a multitude of nephrotoxins (eg., NSAID’s, ACE-Inhibitors, antibiotics) are common complications during hospitalization, which may also explain an increased SCr and associated higher mortality rates.  Newhouse et al[12] found that among 32,161 hospitalized patients not exposed to contrast, 19% of patients had a 25% increase in SCr, which would have fulfilled diagnostic criteria for CIN had they been exposed to IV contrast.

Lipsitch et al[13] stated that non-causal associations between outcomes and exposures are the result of either mismeasurement (recall bias), confounding bias, or selection bias.  To prevent confounding, Lipsitch et al[13] suggests designing a negative control experiment where the observation is repeated under conditions that are not expected to produce the outcome of interest.  If the outcome is encountered without the exposure, then a confounding bias may exist. This form of negative control experiment in which the incidence of AKI is compared across patients exposed and unexposed to contrast has been studied by multiple investigators[14], [15], [16], [17] , all failed to find a statistically significant difference in AKI rate (using CIN definition) between those exposed to contrast and controls.

These studies[18-21] that compared the incidence of CIN between contrast- exposed and unexposed groups also posed methodological issues related to the differences in the baseline risks of AKI between the two study groups.  It is not surprising that the patients hospitalized after requiring a contrast-enhanced CT may be inherently different that those not requiring a similar study.  To account for this potential selection bias, multiple studies have compared the incidence of AKI between contrast exposed and unexposed patients utilized propensity-scoring matching.  Propensity-score matching is a methodology that balances the baseline outcome risks between the study groups[18].  Even utilizing propensity-score matching for AKI, multiple studies[19], [20], [21], [22], [23] again failed to find a statistically higher incidence of AKI in the contrast- exposed compared to unexposed group of hospitalized patients.  In addition, the increases in risks of higher mortality rate in the CIN patients were not found when propensity-scoring matching accounted for the baseline risk of mortality of the contrast-exposed and non-contrast exposed patients.

The most recent CIN study by Hinson et al[1] in this recent issue of Annals of Emergency Medicine represents the latest in the line of investigations into the causal relationship between contrast and AKI.  Hinson et al[1] conducted a retrospective study over a 5-year period comparing the incidence of AKI among three groups, including contrast-enhanced CT (n=7,201), non-contrast enhanced CT (n=5,499), and those in whom CT was not performed (n=5,234).  These three groups were propensity-scoring matched for AKI risks.  AKI was defined both using the common CIN definition and definitions of AKI as reported in the Acute Kidney Injury Network/Kidney Disease Improving Global Outcomes (KDIGO) guidelines[24].   Applying the traditional definition of CIN, AKI was found in 10.6%, 10.2%, and 10.9% in contrast-enhanced CT, non-contrast CT, and non-CT groups, respectively.  Utilizing the KDIGO AKI definitions, AKI occurred in 6.7%, 8.9%, and 8.1% in contrast-enhanced CT, non-contrast CT, and non-CT groups, respectively.

Compared to previous propensity-scoring matched studies mentioned above, Hinson et al[1] went a step further by conducting a multiple logistic regression analysis, including in their model known predictors of AKI and contrast administration. From the multiple logistic regression model, contrast administration produced a non-significant odds-ratio for AKI as defined by both the CIN (0.96 [95% CI, 0.85-1.08]) and KDIGO criteria (1.00 [95% CI, 0.87-1.1.6]).  Moreover, the authors found no differences among the three study groups for the development of chronic kidney disease, need for dialysis, or renal transplantation in the following 6 months post-contrast exposure.

Although patients with elevated SCr (> 4.0 mg/dl) were excluded from their primary analysis, multiple logistic regression analysis of patients with elevated baseline SCr found no independent risk of AKI for contrast administration.

In conclusion, comparing the methodological rigor of more recent CIN studies to those in the past, it seems clear that earlier studies purporting a causal relationship between AKI and contrast administration were only identifying an association but not a true clinical entity. Older CIN studies were biased by confounding variables (e.g., hemodynamic instability, nephrotoxins), with well-established links to AKI providing a sufficient cause for AKI without implicating contrast as an additional AKI risk.

The history of the study of CIN is just another example of evidence-based medicine successfully applied to the debunking of a common belief in a clinical syndrome.  As ED physicians are faced with the challenge of rapidly diagnosing life-threatening conditions (i.e. aortic dissection/aneurysmal rupture, pulmonary embolism, occlusion or aneurysmal rupture of cerebral vessels, traumatic vascular injury), we should not delay emergent contrast-enhanced CT scans waiting for SCr.

 

References / Further Reading

[1] Hinson JS, Ehmann MR, Fine DM, et al. Risk of Acute Kidney Injury After Intravenous Contrast Media Administration. Ann Emerg Med 2017.

[2] Bartels ED, Brun GC, Gammeltoft A, Gjorup PA. Acute anuria following intravenous pyelography in a patient with myelomatosis. Acta Med Scand 1954;150:297-302.

[3] Pickering JW, Blunt IR, Than MP. Acute Kidney Injury and mortality prognosis in Acute Coronary Syndrome patients: A meta-analysis. Nephrology (Carlton, Vic) 2016.

[4] Mitchell AM, Jones AE, Tumlin JA, Kline JA. Prospective study of the incidence of contrast-induced nephropathy among patients evaluated for pulmonary embolism by contrast-enhanced computed tomography. Acad Emerg Med 2012;19:618-25.

[5] Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004;44:1393-9.

[6] Lin KY, Zheng WP, Bei WJ, et al. A novel risk score model for prediction of contrast-induced nephropathy after emergent percutaneous coronary intervention. International journal of cardiology 2017;230:402-12.

[7] Li H, Wang C, Liu C, Li R, Zou M, Cheng G. Efficacy of Short-Term Statin Treatment for the Prevention of Contrast-Induced Acute Kidney Injury in Patients Undergoing Coronary Angiography/Percutaneous Coronary Intervention: A Meta-Analysis of 21 Randomized Controlled Trials. American journal of cardiovascular drugs: drugs, devices, and other interventions 2016;16:201-19.

[8] Wang N, Qian P, Kumar S, Yan TD, Phan K. The effect of N-acetylcysteine on the incidence of contrast-induced kidney injury: A systematic review and trial sequential analysis. International journal of cardiology 2016;209:319-27.

[9] Subramaniam RM, Suarez-Cuervo C, Wilson RF, et al. Effectiveness of Prevention Strategies for Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis. Ann Intern Med 2016;164:406-16.

[10] Grimes DA, Schulz KF. Bias and causal associations in observational research. Lancet 2002;359:248-52.

[11] McNamee R. Confounding and confounders. Occup Environ Med 2003;60:227-34; quiz 164, 234.

[12] Newhouse JH, Kho D, Rao QA, Starren J. Frequency of serum creatinine changes in the absence of iodinated contrast material: implications for studies of contrast nephrotoxicity. AJR Am J Roentgenol 2008;191:376-82.

[13] Lipsitch M, Tchetgen Tchetgen E, Cohen T. Negative controls: a tool for detecting confounding and bias in observational studies. Epidemiology 2010;21:383-8.

[14] Cramer BC, Parfrey PS, Hutchinson TA, et al. Renal function following infusion of radiologic contrast material. A prospective controlled study. Arch Intern Med 1985;145:87-9

[15] Heller CA, Knapp J, Halliday J, O’Connell D, Heller RF. Failure to demonstrate contrast nephrotoxicity. Med J Aust 1991;155:329-32.

[16] Bruce RJ, Djamali A, Shinki K, Michel SJ, Fine JP, Pozniak MA. Background fluctuation of kidney function versus contrast-induced nephrotoxicity. AJR Am J Roentgenol 2009;192:711-8.

[17] Sinert R, Brandler E, Subramanian RA, Miller AC. Does the current definition of contrast-induced acute kidney injury reflect a true clinical entity? Acad Emerg Med 2012;19:1261-7.

[18] Haukoos JS, Lewis RJ. The Propensity Score. JAMA 2015;314:1637-8.

[19] Davenport MS, Khalatbari S, Dillman JR, Cohan RH, Caoili EM, Ellis JH. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology 2013;267:94-105.

[20] McDonald RJ, McDonald JS, Carter RE, et al. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology 2014;273:714-25.

[21] Hsieh MS, Chiu CS, How CK, et al. Contrast Medium Exposure During Computed Tomography and Risk of Development of End-Stage Renal Disease in Patients With Chronic Kidney Disease: A Nationwide Population-Based, Propensity Score-Matched, Longitudinal Follow-Up Study. Medicine 2016;95:e3388.

[22] Tremblay LN, Tien H, Hamilton P, et al. Risk and benefit of intravenous contrast in trauma patients with an elevated serum creatinine. J Trauma 2005;59:1162-6; discussion 6-7.

[23] Cely CM, Schein RM, Quartin AA. Risk of contrast induced nephropathy in the critically ill: a prospective, case matched study. Critical care (London, England) 2012;16:R67.

[24] Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2:1-138.

Acute Angle Closure Glaucoma: ED-Relevant Management

Authors: Colton Langridge, MD (EM Resident Physician, UTSW / Parkland Memorial Hospital) and Dustin Williams, MD (EM Attending Physician / APD, UTSW / Parkland Memorial Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

Case

A 65-year-old female of Vietnamese descent with past medical history of hypertension and diabetes mellitus type 2 presents with acute onset right sided headache that began while reading in dim light 3 hours prior to arrival. The location of the pain is in the peri/retroorbital region on the right and radiates to the right temple. She is seeing halos around lights and has vomited twice on the way to the ED. She has never had a headache of this quality in the past. The remainder of her review of systems is negative, including trauma. She has a history of “sulfa allergy” 5 years ago while taking Bactrim in which she developed hives and shortness of breath.

She is hypertensive, while the remainder of her vital signs are unremarkable. On exam, she has scleral injection, a hazy cornea, and mid-dilated, fixed pupil. The globe itself feels rock hard on palpation. There is no proptosis or palpable cord in the R temporal region. Extraocular muscles are intact, and she has a normal neurological exam including no meningismus.

Visual acuity is performed, and she has 20/80 OS and 20/200 OD. Her baseline is 20/80 in each eye, and she does wear reading glasses. Her fluorescein stain reveals no abnormal uptake. Fundoscopic exam is difficult due to corneal haziness. Tonometry in the L eye shows a pressure of 28 mmHg. The pressure in her R eye is elevated to 72 mmHg.

Timolol and brimonidine eye drops are ordered and administered with repeat tonometry performed every 30 minutes, while awaiting ophthalmology’s arrival. Her OD pressure consistently drops until her IOP is under 35 mmHg. Ophthalmology recommends starting topical steroids and informs you that they plan to perform Laser Peripheral Iridotomy in the next 24 to 48 hours after the haziness in her cornea subsides.

Introduction

Acute angle closure glaucoma (AACG) is the acute elevation of intraocular pressure due to diminished outflow of aqueous humor through the anterior chamber of the eye into the peripherally located canal of Schlemm. It occurs in 1 in 1000 whites and as frequently as 1 in 100 Asians. It occurs even more frequently in those of Inuit descent with estimates of 2-4 in 100 (1). The importance of this disease entity lies in its proclivity to cause optic nerve ischemia. As a result, AACG can lead to visual impairment or blindness if not treated early and appropriately.

Pathophysiology

Aqueous humor is produced by the ciliary epithelium covering the ciliary body in the posterior chamber of the eye. Production is under the control of sympathetic β receptors. After production, aqueous humor flows from the posterior chamber, then between the angle of the lens and iris, through the pupil into the anterior chamber, and finally into the trabecular meshwork located anterior to the ciliary body at the junction of the cornea and sclera. From the trabecular meshwork, aqueous humor flows through the canal of Schlemm where it is resorbed. Two types of acute angle closure glaucoma exist; primary and secondary. Primary AACG occurs in the absence of a precipitating event or insult. In Primary AACG aqueous humor is restricted from flowing through the more anteriorly located pupil due to the posterior iris becoming attached to the lens behind it causing diminished outflow. (6) As aqueous humor accumulates, the iris is pushed forward, especially at its peripheral margin, causing a bowing effect that then causes impingement on the trabecular network and canal of Schlemm.  This further restricts outflow. Patients who already have shallow anterior chambers are particularly at risk, as the angle between the peripheral iris and trabecular meshwork is already narrow and predisposed to sudden closure. Those of Asian (especially Inuit descent) and women tend to have a more narrow anterior chamber, which increases the risk of developing AACG.

There are many precipitants that can contribute to the development of AACG. A classic story is the acute onset of eye pain after walking into a movie theater (i.e. a dimly lit room). Reading in dim light can also precipitate AACG. Sympathomimetics and anticholinergics can both cause pupillary dilatation and thus AACG.

Diagnosis

AACG, for the emergency physician, is a clinical entity that is diagnosed based on a combination of clinical suspicion and exam findings. IOP as detected by applanation tonometry will be elevated. Acute onset eye pain and a minimally reactive mid-dilated pupil with elevated intra-ocular pressure (usually greater than 30 mmHg) is highly suggestive of AACG.

In recent years, more formal criteria have been used to diagnose AACG. These criteria include at least 2 of the following complaints/symptoms: ocular pain, a history of intermittent visual blurring which may include the complaint of seeing halos, and nausea or vomiting. At least 3 of the following signs are required: IOP greater than 21 mm Hg, corneal edema, conjunctival injection, a mid-dilated minimally reactive pupil, and a shallow anterior chamber (11).

A narrow anterior chamber can be determined by oblique flashlight test. This test is performed by shining a flashlight tangentially in a lateral to medial direction across the patient’s eye in a dark room. If there is a shadow over the medial aspect of the iris then the anterior chamber is narrow (5).

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From: http://littlewhitecoats.blogspot.com/2010/12/what-is-oblique-flashlight-test.html

Consultation

An immediate ophthalmology consultation should be made once the Emergency physician suspects this diagnosis. As more time elapses, more optic nerve atrophy will occur (10).

Treatment

In the acute setting, the goal is to emergently reduce IOP, not to perform definitive therapy. This can be started before ophthalmology arrives. Several types of eye drops and a few intravenous medications are effective in rapidly reducing IOP. Most of these medications used for one of the following two mechanisms: increasing aqueous humor outflow or reducing production of aqueous humor altogether. The particular medication regimen that is chosen should be tailored based on a patients’ past medical history and previous drug allergies. The table below summarizes the various medication choices frequently chosen in the acute management of AACG.

Medication Class Medication Pharmacology Adverse Effects/Cautions
Beta Blockers Timolol 0.5% Decrease production of aqueous humor Systematically absorbed/caution in asthma/COPD
Alpha 2 Agonists Brimonidine 0.15% Decrease production of aqueous humor and increase outflow
Carbonic Anhydrase Inhibitors Acetazolamide (Diamox) 500 mg IV or PO Decrease production of aqueous humor Sulfa drug; Use caution in Sulfa allergic patients; Avoid in patients with Sickle cell disease (increased sickling)
Prostaglandin Analogs Latanoprost 0.005% Increase aqueous humor outflow Browning of the iris
Muscarinic Agonists Pilocarpine 1-2% Increase aqueous humor outflow

 

Ineffective at high IOP
Topical Steroids Prednisolone 1% Decrease inflammation and synechiae formation Use in conjunction with ophthalmology
Desiccating Agents/Hyperosmotic Agents Mannitol 1-2g/kg IV Draw fluid out of the vitreous humor by osmotic pressure Caution with use in patients with intravascular volume depletion

*Because aqueous humor production is stimulated by β receptors, β blockers are effective in decreasing further production of aqueous humor. Timolol functions in this way.

*Alpha 2 receptors in the eye (as elsewhere in the body) inhibit sympathetic stimulation. Alpha 2 agonism functions to decrease aqueous humor production by reducing sympathetic outflow and thereby decreasing the β mediated aqueous humor production. Alpha 2 agonism also decreases the mydriatic effect of sympathetic stimulation on the iris through alpha 1 receptors. Brimonidine functions in this manner.

*Carbonic anhydrase is an enzyme that is used in erythrocytes and in the renal tubule for bicarbonate/CO2 titration and/or buffering effects. In the eye it is used for aqueous humor production. Inhibition of this enzyme minimizes production through this pathway. Acetazolamide functions in this way.

*Prostaglandin analogs are thought to increase aqueous humor outflow without affecting its production. One proposed mechanism suggests that they work by altering the production of matrix metalloproteinases. These are thought to cause changes in the extracellular matrix of the iris and widening of connective tissue filled spaces. (4)

*Muscarinic agonists cause miosis. This may help pull the posterior iris from the lens, thereby helping to increases aqueous humor outflow through the pupil. Pilocarpine works by this mechanism. Unfortunately, under high intraocular pressure settings, pilocarpine is less effective. This is because during these conditions, pressure induced ischemic paralysis of the iris decreases its effectiveness. There is also concern that by constricting the ciliary muscles, pilocarpine may increase the axial thickness of the lens and cause anterior displacement, which may reduce the depth of the anterior chamber effectively worsening outflow of aqueous humor. Pilocarpine should be given after other eye drops.

*Topical steroids decrease the overall inflammatory response and scar tissue/synechiae formation.

*Mannitol works by drawing water out of the vitreous humor by osmotic means, thereby decreasing the overall fluid in the eye, dropping the pressure.

*It’s important to give adequate pain control with opioids such as morphine or fentanyl. Antiemetics should be given for nausea and vomiting.

Start with a topical β blocker and alpha 2 agonist +/- diamox. Diamox can be given by mouth if IOP is not excessively elevated (i.e. less than 40). If highly elevated, IV Diamox is preferred. Topical pilocarpine can be considered but should be used with caution 1-2 hours after IOP is reduced for the reasons stated earlier. If IOP is not significantly reduced by 25% at 30-60 minutes, an osmotic agent should be strongly considered. The goal IOP should be 35 or less (3).

If IOP is not effectively reduced in a timely manner, corneal indentation (CI) can be considered (9). This is performed by indenting the cornea with a soft instrument (i.e. cotton tipped applicator) after administration of a topical anesthetic. By indenting the cornea, aqueous humor is displaced peripherally, opening the angle and increasing aqueous outflow temporarily.

Definitive therapy is performed by ophthalmology by means of Laser Peripheral Iridotomy (LPI). Ideally, this is performed within 24 to 48 hours. However, LPI must be performed under circumstances in which visibility is optimal. In many cases of AACG, corneal haziness impairs visibility. Once IOP is reduced, water is drawn out of the cornea and visibility improves, thus allowing LPI to be performed. LPI may need to be performed on the consensual eye in order to prevent AACG in that eye as well.

Disposition

Disposition should be made in conjunction with ophthalmology. There should be a low threshold for admission, especially for those who receive osmotic diuretics, as they may require further electrolyte monitoring. For those who will follow up as outpatients, patients must be able to reliably follow up in an ophthalmology clinic within the next 24-48 hours. In addition, they should be discharged with topical IOP lowering agents, as definitive therapy (LPI) will not have been performed yet.

Summary

  1. Consider AACG in all patients presenting with headache and visual changes, especially if associated with nausea and vomiting.
  2. AACG occurs more frequently in females and those of Asian descent.
  3. Early and effective therapy is vital in reducing optic nerve ischemia and vision loss. Time is optic nerve.
  4. Be aware of the patient’s comorbidities and allergies before treating (i.e. be aware of the risks of topical β blockers in COPD/asthma, sulfa allergy with acetazolamide use)
  5. Consider corneal indentation as a temporizing maneuver if IOP is not satisfactorily lowered in a reasonable amount of time.
  6. There is no emergent treatment that an ophthalmologist can offer that an emergency physician cannot. Definitive treatment is with LPI, however this is frequently delayed until corneal clearing occurs. Thus topical and IV agents are paramount in early treatment of AACG.

 

References / Further Reading

  1. He M, Foster PJ, Ge J, Huang W, Zheng Y, Friedman DS. Prevalence and clinical characteristics of glaucoma in adult Chinese: a population-based study in Liwan District, Guangzhou. Invest Ophthalmol Vis Sci. 2006 Jul. 47(7):2782-8.
  2. Ang LP, Ang LP. Current understanding of the treatment and outcome of acute primary angle-closure glaucoma: an Asian perspective. Ann Acad Med Singapore. 2008 Mar. 37(3):210-5.
  3. Singer MS, Salim S. Bilateral acute angle-closure glaucoma as a complication of facedown spine surgery. Spine J. 2010 Sep. 10(9):e7-9.
  4. Toris CB, Gabelt BT, Kaufman PL. Update on the mechanism of action of topical prostaglandins for intraocular pressure reduction. Surv Ophthalmol. 2008 Nov;53 Suppl1:S107-20.
  5. Coleman AL. Glaucoma. The Lancet; Nov 20, 1999; 354, 9192
  6. Tarongoy P, Lin C, Walton D. “Angle-closure Glaucoma: The Role of the Lens in the Pathogenesis, Prevention, and Treatment”. Survey of Ophthalmology, Volume 54   Number 2 2009.
  7. Choong YF, Irfan S, Menage M. Acute angle closure glaucoma: an evaluation of a protocol for acute treatment. Eye (1999) 13, 613-616.
  8. Emanuel ME et al. Evidence-based management of primary angle closure glaucoma. Curr Opin Ophthalmol 2014, 25:89–92.
  9. Masselos K, Bank A, Francis IC, Stapleton F. Corneal indentation in the early management of acute angle closure. Ophthalmology. 2009 Jan. 116(1):25-9.
  10. Weizer J. Angle-Closure Glaucoma. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on August 5 2016.)
  11. Khondkaryan Ani, Francis Brian A. Angle Closure Glaucoma. American Academy of Ophthalmology. https://www.aao.org/munnerlyn-laser-surgery-center/angleclosure-glaucoma-19. Dec18, 2013.