Diagnosis on Sight: “I have a rapid heart rate”

A 31-year-old male presented to the emergency department with palpitations. The patient stated that he thinks his symptoms began “last night” and felt like he had “a rapid heart rate.” He said that prior to last night he felt fine. He did admit to drinking alcohol with his friends 2 nights prior. The patient estimated that he “must have drunk about 30 beers.” On review of systems, he reported feeling anxious. He denied illicit drug use, headache, chest pain, cough, shortness of breath, fevers, nausea, vomiting, abdominal pain, dysuria, or increased urinary frequency. He reported that he was unaware of any family history of early heart disease or sudden death. His initial EKG is shown below.

After consultation with cardiology, the decision was made to cardiovert the patient given the wide complex tachycardia. After cardioversion, the resulting EKG is shown below:

On review of previous records, the patient had a recent ED visit 2 months ago with the EKG shown below:

What is the diagnosis?

Preexcited atrial fibrillation with underlying Wolf-Parkinson-White syndrome

Explanation:

Wolf-Parkinson-White (WPW) syndrome and the WPW pattern on EKG are rare disorders. Only 0.13 – 0.25% of the population have a WPW pattern on EKG [1,2]. However, only a small fraction of these people will develop WPW syndrome. WPW syndrome is defined as a symptomatic arrhythmia with a WPW pattern on EKG.

The patient’s initial EKG showed a wide complex tachycardia that was ultimately determined to be preexcited rapid atrial fibrillation. After cardioversion, the patient’s underlying baseline EKG tracing showed findings of Wolf-Parkinson-White with:

A shortened PR interval
Widened QRS complex
Delta wave: Slurred upstroke of the QRS complex

The most common arrhythmias associated with WPW syndrome are:

AV Reentrant Tachycardia (AVRT): Seen in over 90% of patients with WPW syndrome [3,4]
Atrial Fibrillation: 10-30% [5,6]
Atrial Flutter: Less than 5%

As in this case, AVRT (i.e. SVT) is often followed by atrial fibrillation in patients with WPW. Although the pathophysiology is unclear, up to 35% of instances of atrial fibrillation were preceded by AVRT [5,7,8].

Fortunately, fatal dysrhythmias such as ventricular fibrillation and ventricular tachycardia are very rare with WPW.

Case Conclusion:

Following cardioversion, the patient remained stable in sinus rhythm. After consultation with cardiology, the patient was discharged on Flecainide and Metoprolol and a referral for outpatient cardiology was placed for follow-up care. Soon after, the patient had an electrophysiology study that showed a left posterolateral accessory conduction pathway. He then underwent successful ablation of his orthodromic AVRT.

Want more visual stimulation? Check out the Diagnose on Sight archives!

References:

Krahn AD, Manfreda J, Tate RB, et al. The natural history of electrocardiographic preexcitation in men. The Manitoba Follow-up Study. Ann Intern Med 1992; 116:456. PMID: 1739235
Kobza R, Toggweiler S, Dillier R, et al. Prevalence of preexcitation in a young population of male Swiss conscripts. Pacing Clin Electrophysiol 2011; 34:949. PMID: 21453334
Josephson ME. Preexcitation syndromes. In: Clinical Cardiac Electrophysiology, 4th, Lippincot Williams & Wilkins, Philadelphia 2008. p.339.
Chugh A, Morady F. Atrioventricular reentry and variants. In: Cardiac electrophysiology from cell to bedside, 5th edition, Zipes DP, Jalife J (Eds), Saunders/Elsevier, Philadelphia 2009. p.605-614.
Campbell RW, Smith RA, Gallagher JJ, et al. Atrial fibrillation in the preexcitation syndrome. Am J Cardiol 1977; 40:514. PMID: 910715
Sharma AD, Klein GJ, Guiraudon GM, Milstein S. Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: incidence after surgical ablation of the accessory pathway. Circulation 1985; 72:161. PMID: 4006127
Sung RJ, Castellanos A, Mallon SM, et al. Mechanisms of spontaneous alternation between reciprocating tachycardia and atrial flutter-fibrillation in the Wolff-Parkinson-White syndrome. Circulation 1977; 56:409. PMID: 884796
Fujimura O, Klein GJ, Yee R, Sharma AD. Mode of onset of atrial fibrillation in the Wolff-Parkinson-White syndrome: how important is the accessory pathway? J Am Coll Cardiol 1990; 15:1082. PMID: 2312962

By Garrett Yee, MD|2021-08-27T09:10:41-07:00Aug 25, 2021|Cardiovascular, Diagnose on Sight, ECG|

SAEM Clinical Image Series: A Recurring Neck Mass

A 30-year-old female with no significant past medical history presents to the Emergency Department with a six-day history of an enlarging, tender, red “bump” on her anterior neck. She reports similar swelling during bouts of pharyngitis. She also reports a recent upper respiratory infection one week ago that was marked by fever, cough, congestion, sore throat, and myalgia. She denies shortness of breath, neck trauma, travel, or animal exposures.

Physical Exam

Vitals: T 37°C; BP 122/78; HR 77; RR 17

General: Well-developed, well-nourished female in no acute distress

HEENT: 2cm tender, fluctuant, mobile right anterior neck mass with surrounding erythema; no drainage noted; mass does not move with swallowing

The remainder of the exam is unremarkable.

Laboratory Data

Non-contributory

Case Question: What is the diagnosis?

Second branchial cleft cyst

Branchial cleft anomalies are the second most common type of congenital neck mass and present as cartilaginous remnants, sinuses, fistulas, or cysts due to the failure of the branchial apparatus to obliterate. The most common are second branchial cleft anomalies, representing 95% of these cases. Second branchial cleft anomalies are usually located along the anterior border of the sternocleidomastoid muscle on the left side of the neck.

Differential diagnoses include thyroglossal duct cyst, neck abscess, cystic hygroma, cervical lymphadenopathy, metastatic lymph nodes, and cat scratch disease.

Case Question: What is the gold standard of treatment for this condition?

The gold standard of treatment necessitates complete surgical excision of the entire branchial cleft anomaly. Branchial cleft anomalies are most commonly diagnosed with computerized tomography (CT) that shows a uniformly hypo-or-anechoic mass with well-defined margins and thin walls. Preoperative fine needle aspiration cytology can be used to view histopathological findings of the mass and help to rule out malignant disease. Ultrasound and MRI can also be helpful for diagnosis, preoperative localization, and preoperative identification of surrounding structures. However, for definitive diagnosis, surgical excision of the entire anomaly and pathology examination is required. If full resection is not achieved, recurrence is possible.

Case Discussion

Take-Home Points

A branchial cleft anomaly is the second most common type of congenital neck mass.
Branchial cleft anomalies are due to failure of the branchial apparatus to obliterate and can present as cartilaginous remnants, sinuses, fistulas, or cysts.
The gold standard of treatment requires complete surgical excision of the entire branchial cleft anomaly to prevent recurrence.

References

Muller S, Aiken A, Magliocca K, Chen AY. Second Branchial Cleft Cyst. Head Neck Pathol.2015;9(3):379-383. doi:10.1007/s12105-014-0592-y Zaifullah S, YunusMR, See GB. Diagnosis and treatment of branchial cleft anomalies in UKMMC: a 10-year retrospective study. Eur Arch 2013;270(4):1501-1506. doi:10.1007/s00405-012-2200-7

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2021 SAEM Annual Meeting | Copyrighted by SAEM 2021 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By Alicia Hereford|2021-08-20T09:57:47-07:00Aug 23, 2021|HEENT, SAEM Clinical Images|

Background

Bleeding patients or those undergoing procedures that are at high risk of bleeding may require correction of their INR. Multiple products can be used to achieve this, including fresh frozen plasma (FFP). FFP contains many substances, including clotting factors, fibrinogen, plasma proteins, electrolytes, and anticoagulant factors. It is sometimes said that the intrinsic INR of FFP is approximately 1.6-1.7 and that it’s not possible to achieve a lower INR. This pearl will further explore these concerns.

Evidence

What is the INR of FFP?
- The mean INR of FFP appears to be ~1.1 (0.9-1.3) [1,2].
- Reports that the intrinsic INR of FFP is 1.6-1.7 may be based on the clinical experience of not being able to achieve an INR <1.6-1.7 with FFP.
Is it possible to “normalize” the INR with FFP alone?
- Several studies have found that it’s difficult to achieve an INR <1.7 with only FFP [3,4]. However, other studies were able to achieve lower average INR values [2,5,6].
- Overall, these studies found that there was a significantly greater decrease in INR when the pre-FFP INR was higher, but there was a much smaller decrease when the INR was closer to the normal range.
Why does FFP appear to have diminishing returns when the pre-FFP INR is lower?
- The relationship between the INR and percentage of clotting factors present in the blood is not linear (see figure) [7].
- For example: An increase of ~5% in clotting factors may decrease the INR from 3 to 2.5 but the same amount of FFP may only reduce an INR of 1.7 to 1.6.

Figure 1: Adapted from Dzik 2012 [7].

- Additionally, the table below also demonstrates that small volumes of FFP result in large changes when the initial INR is elevated, but very large amounts of FFP are required to achieve an INR of 1.3 no matter the initial INR (see table).

Amount of FFP to Achieve a Target INR Based on Pre-FFP INR
Target INR
	1.3			1.7			3.0
Initial INR	Volume (L)	Dose (mL/kg)	Factor (%)	Volume (L)	Dose (mL/kg)	Factor (%)	Volume (L)	Dose (mL/kg)	Factor (%)
6.0	4.5	64	45	2.5	36	25	1.5	21	15
5.0	4.3	61	43	2.3	32	23	1.0	14	10
4.0	4.0	57	40	2.0	29	20	0.5	7	5
3.0	3.5	50	35	1.5	21	15	–	–	–
2.0	2.5	36	25	0.5	7	5	–	–	–

Table 1: Adapted from Holland 2006 [3]. Note: 1 unit of FFP is ~200-250 mL

- Given the above data, the issue preventing the achievement of an INR <1.7 appears to be the dose/volume of FFP required and not the intrinsic INR of FFP.

Does the INR need to be <1.7 to achieve hemostasis?
- Since the INR only provides limited information regarding a single aspect of anticoagulation status, complete normalization for the INR to control bleeding is usually not necessary [6].
- An INR elevation alone does not indicate a patient is coagulopathic or at an increased risk of bleeding [7]. Additionally, an INR elevation in patients with liver dysfunction likely reflects an overall state of decreased factor production, both procoagulant and anticoagulant factors [8].
- The target INR varies depending on multiple patient factors and planned interventions, but an INR of 1.0 is likely not necessary to prevent bleeding or achieve hemostasis.

Bottom Line

A unit of FFP has an INR of ~1.1, but this doesn’t mean it can easily normalize the INR.
There is a non-linear relationship between percentage of clotting factors and the INR, resulting in diminishing returns from each unit of FFP as the INR decreases.
Very large doses of FFP may be required to fully correct an elevated INR, which frequently precludes its use.
Complete normalization of the INR is not required to achieve hemostasis or prevent bleeding from a procedure.

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

Holland LL, Foster TM, Marlar RA, Brooks JP. Fresh frozen plasma is ineffective for correcting minimally elevated international normalized ratios. Transfusion. 2005;45(7):1234-1235. doi: 10.1111/j.1537-2995.2005.00184.x. PMID: 15987373.
Only AJ, DeChristopher PJ, Iqal O, Fareed J. Restoration of normal prothrombin time/international normalized ratio with fresh frozen plasma in hypocoagulable patients. Clin Appl Thromb Hemost. 2016;22(1):85-91. doi: 10.1177/1076029614550819. PMID: 25294634.
Holland LL, Brooks JP. Toward rational fresh frozen plasma transfusion: The effect of plasma transfusion on coagulation test results. Am J Clin Pathol. 2006;126(1):133-139. doi: 10.1309/NQXH-UG7H-ND78-LFFK. PMID: 16753596.
Abdel-Wahab OI, Healy B, Dzik WH. Effect of fresh-frozen plasma transfusion on prothrombin time and bleeding in patients with mild coagulation abnormalities. Transfusion. 2006;46(8):1279-1285. doi: 10.1111/j.1537-2995.2006.00891.x. PMID: 16934060.
Müller MCA, Straat M, Meijers JCM, et al. Fresh frozen plasma transfusion fails to influence the hemostatic balance in critically ill patients with a coagulopathy. J Thromb Haemost. 2015;13(6):989-997. doi: 10.1111/jth.12908. PMID: 25809519.
McCully SP, Fabricant LJ, Kunio NR, et al. The International Normalized Ratio overestimates coagulopathy in stable trauma and surgical patients. J Trauma Acute Care Surg. 2013;75(6):947-953. doi: 10.1097/TA.0b013e3182a9676c. PMID: 24256665.
Dzik W “Sunny.” Reversal of drug-induced anticoagulation: old solutions and new problems. Transfusion. 2012;52(s1):45S-55S. doi: 10.1111/j.1537-2995.2012.03690.x. PMID: 22578371.
Harrison MF. The misunderstood coagulopathy of liver disease: a review for the acute setting. West J Emerg Med. 2018;19(5):863-871. doi: 10.5811/westjem.2018.7.37893. PMID: 30202500.

By Mike O'Brien, PharmD|2021-08-28T10:03:39-07:00Aug 21, 2021|EM Pharmacy Pearls, Heme-Oncology|

A 32-year-old female presents to the emergency department with right ankle pain after a high-speed motor vehicle accident. On exam, she is noted to have ecchymosis and swelling over the distal foot, and pain with ankle dorsiflexion and plantarflexion. An x-ray is obtained as shown above (Image 1. Case courtesy of Dr. Charlie Chia-Tsong Hsu, Radiopaedia.org, rID: 18235).

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By Ko, MD, CAQ-SM|2021-08-08T12:15:05-07:00Aug 18, 2021|Expert Peer Reviewed (Clinical), Orthopedic, SplintER|

SplintER Series: My Foot Doesn’t Work Right

Achilles tendon rupture

A 35-year-old male felt a painful “pop” in his posterior left lower leg while playing football. Afterward, his “foot didn’t work right anymore.” X-ray of the left ankle and tib/fib was normal but he was unable to ambulate. You plan an ultrasound over the area of maximal tenderness and discover the above image (Image 1.Ultrasound of the left posterior ankle 11cm proximal to the calcaneal insertion of the Achilles tendon. Case courtesy of Robert Lystrup.)

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By Christopher Durkin, DO|2021-07-30T16:03:25-07:00Aug 11, 2021|Expert Peer Reviewed (Clinical), Orthopedic, SplintER|

SAEM Clinical Image Series: Sudden Onset of Facial Petechiae in Kindergartener

petechiae

A 6-year-old boy with no past medical history presented when his parents noticed facial petechiae after picking him up from school. He had a series of four recent upper respiratory infections within four months since starting public kindergarten. He occasionally also complains of leg pain.

Additional Images

Physical Exam

General: Non-toxic, cooperative child

Skin: Petechial rash in periorbital and infra-auricular areas

HEENT: Normal; no lymphadenopathy

Musculoskeletal: Normal strength and range of motion

Laboratory Data

Hemoglobin: 12.6 g/dL

White blood cell (WBC) count: 6.7×10³/mL

Platelets: 352,000/mL

Case Question: What is this most common cause of facial petechiae?

Increased pressure in the dermis from actions such as extended Valsalva maneuver, vomiting, crying, or coughing.

This child had a stressful day in kindergarten. He was holding his breath for extended periods of time to suppress crying. The increased pressure caused the facial petechiae, which was completely unrelated to his recent viral infection or growing pains

Case Discussion

Take-Home Points

Fine petechiae around the eyes, cheeks, and ears are most often caused by crying or similar behaviors that cause increased pressure in the subcutaneous vessels of the face.
Mucosal and cutaneous capillaries are fragile and can easily rupture, even with minor trauma. Usually, platelets can seal these immediately, so when petechiae show up, consider a problem with primary hemostasis.

References

Kumar V, Abbas A, Aster J. Hemodynamic Disorders, Thromboembolic Disease, and Shock. Robbins & Cotran Pathologic Basis of Disease, 10th edition. 2021. Marcdante K, Kliegman R. Immunological Assessment. Nelson Essentials of Pediatrics, 8th edition. 2019

Copyright

By Sara Urquhart|2021-07-22T22:10:34-07:00Aug 9, 2021|Dermatology, HEENT, Pediatrics, SAEM Clinical Images|

SplintER Series: Fracture After a Fall From a Bunk Bed

A 6-year-old male presents to the ED after a fall from his 5 foot high bunk bed causing elbow trauma. On exam, there is significant focal swelling, ecchymosis, and tenderness at the lateral left elbow. The forearm, wrist, hand and shoulder are nontender. He is neurovascularly intact. You suspect a fracture and obtain x-rays (Figures 1 and 2).