Community EM

Fibrinolytic Therapy for STEMI

Case

You are on a swing shift at a remote, island-based community hospital when a 58 year-old male presents with sudden onset chest pain. The pain started at rest, radiates to his jaw, and is associated with diaphoresis and nausea. He has a history of coronary artery disease (CAD), and during his last cardiac catheterization in 2008, a stent was placed in his proximal left anterior descending coronary artery. His past medical history is also significant for diabetes, chronic obstructive pulmonary disease, hyperlipidemia, and hypertension.  He is an active smoker.

On exam, he is not only diaphoretic and clenching his chest, but also describes the pain as “an elephant sitting on my chest.” Initial vital signs are P 110, BP 175/100, RR 20, PO2 98% on RA, T 98.9 F. You give him aspirin 324 mg and nitroglycerin sublingual 0.4 mg, and his chest pain improves from a 10/10 to 8/10. His initial electrocardiogram (EKG) is below.

Figure 1: The patient’s presenting EKG.

Figure 1: The patient’s presenting EKG.

DIAGNOSIS

ST elevation myocardial infarction (STEMI)

Management Options

You call the critical care transport ambulance, as well as the nearest cardiac catheterization team to alert them of your patient.   Unfortunately, it is a stormy evening in the middle of winter and all bridges off the island are closed; helicopters are grounded due to the storm.  There are no transfer options available to your patient at this time. What else can you do?

Indications for Fibrinolytic Therapy

According to the American Heart Association, there are several considerations when it comes to fibrinolytic therapy in myocardial infarction:

Class I recommendations:

  1. STEMI

  2. Symptom onset in the last 12 hours

  3. Percutaneous Cardiac Intervention (PCI) cannot be performed within 120 minutes of arrival to the Emergency Department

  4. Absence of any contraindications (see below)

Class II recommendations:

  1. Evidence of ongoing ischemia 12-24 hours after symptom onset

  2. Large area of myocardium affected

  3. Hemodynamic instability

Absolute contraindications:

  1. Any prior intracranial hemorrhage

  2. Known structural cerebral vascular lesion

  3. Ischemic stroke <3 months

  4. Suspected aortic dissection

  5. Known intracranial malignancy

  6. Active bleeding or bleeding diathesis

  7. Significant closed head trauma <3 months

  8. Intracranial/intraspinal surgery <2 months

  9. Severe uncontrolled HTN (>175/110)

  10. Oral anticoagulants

Relative contraindications:

  1. Significant HTN on arrival (pressure > 180 mmHg)

  2. Ischemic stroke >3 months

  3. Dementia

  4. Other intracranial pathology

  5. Traumatic CPR >10 min

  6. Major surgery <3 weeks

  7. Internal bleeding <3 weeks

  8. Non-compressible vascular punctures

  9. Pregnancy

  10. Active peptic ulcer disease

PCI versus Systemic Fibrinolytic Therapy

If you are able to transfer the patient to a hospital with PCI capability within 1 hour of presentation or they have contraindications to fibrinolytic therapy, it is recommended that you transfer the patient as soon as possible. Otherwise, the goal is fibrinolytic infusion within 30 minutes of arrival to the ER. In either case, concurrently initiate maximal medical management including full-dose aspirin, Plavix or Brilinta, and anticoagulation (unfractionated heparin or lovenox). Tenecteplase is generally the preferred fibrin-specific agent, given its ease of use and lower rates of non-cerebral bleeding compared to other agents.

Reassess After Fibrinolysis

If your patient has resolution of chest pain and >70% reduction of ST elevation, or ST elevation resolves within 60-90 minutes, you have likely restored flow. If you see <50% decrease in STE and no reperfusion arrhythmias (see below) at 2 hours after fibrinolytic dosing, you have partially improved flow but not completely restored it.

Criteria for Transfer after fibrinolytic therapy

  1. Immediate transfer: acute heart failure or cardiogenic shock

  2. Urgent transfer: failed reperfusion or reocclusion

  3. 3-24 hours: hemodynamically stable, successful reperfusion

Reperfusion Arrhythmias 

You plan for ICU admission because you are unable to transfer the patient to a PCI center when the nurse hands you the following EKG:

Figure 2: Accelerated idioventricular rhythm.

Figure 2: Accelerated idioventricular rhythm.

This is an example of accelerated idioventricular rhythm. This is a normal sign of reperfusion after STEMI and does not require treatment.   In fact, such a rhythm is generally viewed as a positive response to fibrinolytic therapy as indicates reperfusion. 

Criteria:

  1. Regular rhythm

  2. Rate 50-110bpm (slower is ventricular escape, faster is VT)

  3. Three or more ventricular complexes

  4. Fusion (F) and capture (C) beats (see below)

Figure 3: Fusion and capture beats after successful reperfusion.

Figure 3: Fusion and capture beats after successful reperfusion.

General goals of care after fibrinolytic therapy should be to transfer for diagnostic angiography and percutaneous coronary evaluation which is promptly accomplished for your patient the following day after the storm resolves.


Faculty reviewer: Dr. Kristina McAteer


References

  1. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:529.

  2. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:e362.

  3. White HD. Thrombolytic therapy in the elderly. Lancet 2000; 356:2028.

  4. Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med 2013; 368:1379.

  5. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Lancet 1986; 1:397.

  6. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet 1988; 2:349.
    Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Lancet 1994; 343:311.

  7. Labinaz M, Sketch MH Jr, Ellis SG, et al. Outcome of acute ST-segment elevation myocardial infarction in patients with prior coronary artery bypass surgery receiving thrombolytic therapy. Am Heart J 2001; 141:469.

  8. Peterson LR, Chandra NC, French WJ, et al. Reperfusion therapy in patients with acute myocardial infarction and prior coronary artery bypass graft surgery (National Registry of Myocardial Infarction-2). Am J Cardiol 1999; 84:1287.

  9. Karnash SL, Granger CB, White HD, et al. Treating menstruating women with thrombolytic therapy: insights from the global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries (GUSTO-I) trial. J Am Coll Cardiol 1995; 26:1651.

  10. Woodfield SL, Lundergan CF, Reiner JS, et al. Angiographic findings and outcome in diabetic patients treated with thrombolytic therapy for acute myocardial infarction: the GUSTO-I experience. J Am Coll Cardiol 1996; 28:1661.

  11. Mak KH, Moliterno DJ, Granger CB, et al. Influence of diabetes mellitus on clinical outcome in the thrombolytic era of acute myocardial infarction. GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol 1997; 30:171.

Meeting Uncle Rhabdo

rhabdo.png

THE PATIENT:

A 28 year old previously healthy male presents to the emergency department with concerns for worsening back pain that is predominantly left sided and along the lumbar spine. Two days prior to the visit he recalls a work out that consisted of many dead lifts. He also played basketball the following day and rode his bike into work, which is more activity than usual for him. He tried NSAIDs for pain control, but his pain is more intense and he noticed his urine looked brown today. He denies any fevers, history of IVDU, weight gain or loss, urinary tract infections or STDs, immunosuppression, recent spinal fracture or procedure, incontinence or retention.

PHYSICAL EXAMINATION:

144/83, 82, 37.1, 18, 98%

Gen: well appearing, no acute distress

HENT: normocephalic, MMM

CV: RRR

Pulm: CTAB

Abd: soft, nontender, nondistended

MSK: muscle spasms along the left lumbar paraspinal muscle, no midline tenderness to palpation, muscle compartments in the upper and lower extremities are soft

Neuro: L1-S5 strength 5/5 and sensation to light touch is intact

Skin: pink, warm, dry

THE COURSE:

As an experienced clinician you are able to quickly arrive at a diagnosis of rhabdomyolysis from the brief history and physical exam, but what else needs to be done? In the emergency department we need to initiate diagnostic studies to evaluate the severity of illness and help plan for an appropriate disposition. Thankfully, your history and exam reveal no red flag findings for more concerning etiologies of back pain, so your evaluation can be quite focused. The patient had lab work sent off and was provided with IVF boluses and given analgesia with marked improvement in his symptoms. He was admitted to the medical floor for continued care for the next couple days.

THE WORK UP:

CK >20,000 IU/L (labs upper limit for reporting without further analysis and quantitative estimates, normal range 20-210, remained >20,000 for 5 consecutive days) finally on day 6 CK 10, 933 IU/L

BMP: Glu 113, BUN 19, Cr 1.0 (on discharge was 0.84), Na 139, K 3.8, Cl 104, CO2 29, Ca 8.9

Urinalysis: Brown, cloudy, trace ketones, specific gravity >1.03, blood 3+, protein >300

Urine microscopic analysis: RBC none seen, WBC 3, amorphous crystals present

Urine myoglobin: >8,750 mcg/ml (normal range < 28mcg/ml)

DISCUSSION:

The key clinical manifestations of rhabdomyolysis include a triad of muscle tenderness and weakness as well as dark urine, so the triage note already had it set up on a silver platter for you. Remember, however, as with any triad in medicine this classic presentation is rare. Some studies revealed that over half of patients do not report muscle pain or weakness. Rhabdomyolysis occurs due to muscle necrosis and the release of intracellular contents into the circulation. Patients may present with a wide range of symptoms and the most concerning complications include hyperkalemia, renal failure and rarely disseminated intravascular coagulation. Patients who present with concomitant acute kidney injury tend to have worse outcomes and the mechanism of injury is primarily related to the nephrotoxic effects of myoglobin. In an acidic environment myoglobin may precipitate and subsequently damage the kidneys by obstruction of the renal tubules, cause oxidative damage and vasoconstriction.

The etiologies of rhabdomyolysis can be broken up into four broad categories: impaired production or use of ATP, dysfunctional oxygen or nutrient delivery, increased metabolic demand exceeding capacity, and direct myocyte damage. Recently, on EM: RAP Dr. DeLaney argued that this can be further simplified into two broad categories, exertional and non-exertional. Classic cases include trauma patients who have crush injuries but can also occur with heat related illnesses such as heat exhaustion or stroke, or in cases of hyper-kinetic states. Medications implicated in this disease process include antipsychotics and statins as well as others such as illegal drugs like cocaine.

CK levels classically rise within two to twelve hours after the onset of injury and peak within three days. The level should return to baseline within ten days. The diagnosis is often considered if the CK level is above five times the upper limit of normal at presentation, roughly 1,000 IU/L. More discrete categories can also be used to differentiate mild to severe cases based on CK levels, however, it is the degree of renal impairment that likely has the greatest role on patient outcome. Emergency department management includes aggressive IVF hydration with a target urine output of approximately 250 ml/hr and attempts to identify and correct the underlying pathology. Some argue for urinary alkalinization; however, the literature is limited with regards to strong recommendations on this topic. Common electrolyte abnormalities include: hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Disseminated intravascular coagulation can rarely be seen as a result of thromboplastin and prothrombotic agents released from damaged myocytes. Acute kidney injury is more common if the presentation includes a CK >5,000 IU/L and in cases with sepsis, acidosis, or dehydration. Ultimately, most patients do well during their hospital courses and rarely require significant interventions, but mortality may be upwards of 20% in those that present with significant kidney injury noted at the time of presentation, therefore, careful evaluation of the patient’s lab studies and admission for close observation remains the mainstay of treatment.

Faculty Reviewer: Dr. Gita Pensa

SOURCES:

  1. DeLaney, M. “Rhabdomyolysis: Part 1 Diagnosis and Treatment.” www.emrap.org March 2018, 18 (3)

  2. DeLaney, M. “Rhabdomyolysis: Part 2 Disposition.” www.emrap.org March 2018, 18 (3)

  3. Majoewsky, M. “Rhabdomyolysis: C3 Project.” www.emrap.org June 2012, 2 (6)

  4. Sauncy, H. (2017). Don’t Get Broken Up About Muscle Breakdown. In Mattu, A. Marcucci, L. et al (Eds.), Avoiding Common Errors in the Emergency Department: Second Edition (pp. 414-16). Philadelphia: Wolters Kluwer.

Do You 'See More' Fractures? Don’t Overlook 'Seymour' Fractures!

Co-Authors: Dr. Madalene Boyle and Dr. Andrew Beck

Case 1

A 10-year-old male presents to the ED with his parents after his finger was slammed in a car door. His parents are concerned that it’s bleeding and appears deformed. The incident occurred 30 minutes prior to presentation. His parents state that there was “a lot of bleeding.” His past medical history is notable for asthma, and there is no history of fragility fractures, connective tissue disorders, or bleeding diatheses. Physical exam reveals the injury as shown. Flexion of the digit is preserved and extension is limited due to pain and deformity. Neurovascular exam is intact. 

Car door injury to 5th digit.

Car door injury to 5th digit.

Screen Shot 2018-08-24 at 11.41.07 AM.png

An x-ray was taken to assess for fracture and/or foreign body. The original film was unavailable, but an illustrative lateral view is shown(3). No foreign body was noted, but a characteristic injury pattern was observed.


 

Case 2

A 14-year old right-handed football player presents to the community Emergency Department with a right middle finger deformity. Patient was playing football when he went to make a tackle and his finger was crushed beneath another player.  

Screen Shot 2018-08-24 at 11.45.28 AM.png

On exam, his middle finger has dried blood at the base of the nail. The proximal nail appears partially avulsed. His finger appears flexed at the DIP although he is able to fire his extensors/flexors at the DIP.  He has no sensory deficits. 

Image from Azburg, 2013.

Image from Azburg, 2013.

 

The Seymour Fracture

Definition & Epidemiology(1,2): Originally described in 1966 by Seymour, the eponymous Seymour fracture is defined as an open, displaced distal phalangeal fracture with associated nail bed injury. This injury can easily be overlooked as minor trauma to the nail which can have consequences for infection and growth arrest, leading to chronic deformity and loss of function.1 20-30% of phalangeal fractures in children involve the physis, and the long finger is most commonly affected. The mechanism is typically a crush injury in a door. These are Salter-Harris Type 1 or 2 fractures and the nailbed injury is commonly a laceration or plate avulsion. Often, interposition of soft tissue at the fracture site impedes bedside reduction. 

The Seymour fracture will often resemble a mallet finger. For this reason, any pediatric patient with an apparent mallet finger deformity and blood at the nail fold should be evaluated seriously for this fracture. The mallet finger appearance occurs because of an imbalance between the flexor and extensor tendons.  The extensor tendon inserts at the epiphysis of the distal phalanx. The flexor digitorum profundus inserts at the metaphysis.  There is no actual injury to the extensor tendon (as in Mallet finger). The imbalance is created through the physis or fracture site (see image). 


Diagnosis (1,2,3): Physical exam demonstrates a flexed dorsal interphalangeal joint, ecchymosis, swelling, and mallet deformity. The nail plate lies superficial to the eponychial fold which will give the appearance of a longer-than-normal nail.1,2,3 Imaging reveals a fracture through the physis along with other potential fractures. The AP radiographic view may be normal since lateral deviation is not commonly seen. The lateral view is more sensitive and will show a widened physis, displacement, and angulation. It is important not to confuse the presentation for a mallet finger which is the key differential diagnosis. Mallet fractures involve the joint while the Seymour fracture is isolated to the growth plate without epiphyseal displacement. 

...any pediatric patient with an apparent mallet finger deformity and blood at the nail fold should be evaluated seriously for this fracture.


Risks: A Seymour fracture has many associated complications. Based on fracture location, the germinal matrix (responsible for nail production) can become entrapped in the fracture site (See image above). This prevents a simple reduction of the fracture. Additionally, damage to the germinal matrix can cause a permanent nail plate deformity.  If soft tissue becomes incarcerated in the physis, it can cause growth arrest and finger length discrepancy. Importantly, failure to treat Seymour fractures as open fractures can result in infection and even chronic osteomyelitis. 


Management: These are open fractures.  In the ER, it is appropriate to give a dose of parenteral antibiotics. A first generation cephalosporin such as Cefazolin is suitable. Patients should be treated with a short (5-7 day course) of oral antibiotics upon discharge. 
A hand specialist should manage Seymour fractures. Appropriate treatment of Seymour fracture consists of removal of the nail plate, exploration of the fracture site (to ensure no tissue entrapment), thorough irrigation and debridement, and reduction. For unstable fractures, a K-wire through the fracture and DIP is sometimes necessary to maintain this reduction.  The nail bed laceration should be repaired. The nail should be replaced or stented with suture packaging material. 
Younger patients may require anesthesia and an operating room for exploration and adequate treatment. Older patients may be able to have treatment within the department with adequate pain control and local nerve blocks. 
Appropriate management of Seymour Fractures is crucial. A recent review by Reyes (2017) evaluated management and associated complications of Seymour fractures.  There was a much higher rate of infection (both superficial and osteomyelitis) in those patients who do not receive proper treatment.  Emergency Medicine providers must be able to recognize this injury in order to initiate antibiotics and facilitate appropriate consultation with a hand specialist. 

Prognosis (3): As mentioned above, nonoperative management may be possible for minimally displaced Seymour fractures. However, by definition, Seymour fractures are open and displaced, and the majority of these injuries require open reduction and fixation. Functional and cosmetic outcomes at two years are equivalent between operative and nonoperative groups when selected for treatment based on degree of displacement. Major complications include reduced range of motion, nail dystrophy, and digit length discrepancy, all of which can have major functional consequences especially if involving the 2nd or 3rd digits on the dominant hand, or if the patient requires the use of multiple digits for a profession (pianist, artist, and typist). 


Case 1 Resolution

This patient received a bedside nail bed repair with avulsion and replacement of the nail plate, then reduction via hyperflexion followed by traction and extension. The patient was splinted and received operative repair within one week of the injury. 


Case 2 resolution

A hand team was not available at the community hospital. Patient was transferred to the Children’s Hospital where he was treated by the hand team.  He underwent I+D in the ER and reduction/repair. He has since had an uneventful follow-up appointment. 

 

References
1)    Nellans KW, Chung KC. Pediatric Hand Fractures. Hand Clin. 2013 Nov; 29(4): 569–578. doi:  10.1016/j.hcl.2013.08.009. 
2)    Watts E. Seymour Fracture. https://www.orthobullets.com/hand/6000/seymour-fracture# Accessed 11/27/2017.
3)    Krusche-Mandl I, Kottstorfer J, Thalhammer G et. Al. Seymour fractures: retrospective analysis and therapeutic considerations. J Hand Surg Am. 2013 Feb;38(2):258-64. doi: 10.1016/j.jhsa.2012.11.015.
4)    Abzug JM, Kozin SH. Seymour fractures. J Hand Surg Am. 2013;38:2267–2270. 
5)    Reyes BA, Ho CA.  The High Risk of Infection With Delayed Treatment of Open Seymour Fractures: Salter-Harris I/II or Juxta-epiphyseal Fractures of the Distal Phalanx With Associated Nailbed Laceration. J Pediatr Orthop. 2017: 37: 247-253. 
6)    Kattan AE, AlShomer F, Alhujayri AK, Alfowzan M, Murrad KA, Alsajjan H. A case series of pediatric seymour fractures related to hoverboards: Increasing trend with changing lifestyle. International Journal of Surgery Case Reports. 2017: 38: 57-60. 

 

FACULTY REVIEWER/EDITOR: Dr. Kristina McAteer