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An Ominous ECG Sign in Critical Care

Originally published 2020;141:2106–2109

    ECG Challenge

    A 35-year-old woman was admitted to the critical care unit for treatment of septic shock. She had developed an abscess in her right hand and group A streptococcal bacteremia as a result of intravenous drug abuse. A transesophageal echocardiogram detected a vegetation on the tricuspid valve, with mild to moderate regurgitation. Septic emboli to the lungs were evident on computed tomography scan. She was hypotensive (85/55 mm Hg), acidotic (pH 7.18), requiring inotropic support and invasive ventilation. A 12-lead ECG was performed because ST-segment elevation was observed on the cardiac monitor. What is the ECG sign in Figure 1?

    Figure 1.

    Figure 1. The 12-lead ECG recorded in the critical care unit.

    Please turn the page to read the diagnosis.

    Response to ECG Challenge

    The QRS-ST segment in Figure 1 is characteristic of the spiked-helmet sign (SHS). The elevation of the isoelectric line precedes the QRS, followed by a sharp R wave and then convex ST-segment elevation. First described by Littmann et al1 in 2011, this characteristic ECG pattern was named for its resemblance to the Prussian military helmet, the Pickelhaube (Figure 2). The 12-lead distribution was initially described only in the inferior leads,1 but the pattern can be widespread as is evident in this case.

    Figure 2.

    Figure 2. Spiked-helmet sign named for its resemblance to the Prussian military helmet, the Pickelhaube.

    The mechanism of this ECG sign is not fully understood. SHS was first detected in cases of acute abdomen and thoracic pathology.1,2 As a result, it was postulated that the ECG pattern was an artifact from the voltage generated by mechanical epidermal stretch caused by a rapid increase in intra-abdominal or thoracic pressure.1,2 However, subsequent reports demonstrated SHS in cases of intracranial hemorrhage, sepsis, and metabolic derangement.2 A unifying explanation emerged in that SHS was caused by adrenergically mediated prolongation of repolarization.2 Such conditions were established causes of acquired long QT.2 SHS may be an extreme manifestation.2 The characteristic pattern may be formed by the preceding beat’s late and giant T-U waves superimposed on the QRS.2 The hypothesis of a hyperadrenergic state was further supported by the detection of SHS after stellate ganglion ablation.2 Furthermore, macroscopic T-wave alternans and torsade de pointes are associated features of both long QT and SHS.2 Given the shared pathophysiology of adrenergic excess, concomitant takotsubo cardiomyopathy has also been described.2

    SHS mimics acute myocardial infarction. However, the upward shift preceding the QRS that can appear to align with the ST-segment elevation is not consistent with acute coronary syndrome.1,2 Aforementioned causes of SHS should first be considered, in particular, intracranial hemorrhage, before antithrombotic drugs are administered as part of acute coronary syndrome protocol. Our patient’s ECG progressively resolved within 24 hours as she responded to antibiotics and supportive measures (Figure 3). Note the absence of Q waves or T-wave inversion that is typical of ECG evolution after ischemic ST-segment elevation.1,2 Cardiac enzymes were not significantly elevated in this case. SHS is the most recent addition to the differential diagnoses of pseudo–ST-segment elevation myocardial infarction pattern. Better recognized causes include pericarditis, bundle-branch block, hypertrophy, hyperkalemia, hypercalcemia, large pulmonary embolism, postcardioversion, digoxin toxicity, early repolarization, and Brugada syndrome.3 These were also considered in our case but were inconsistent with the available clinical, ECG, laboratory, and imaging findings at the time.

    Figure 3.

    Figure 3. Progressive resolution of patient’s ECG within 24 hours.A, Spiked-helmet sign becomes less pronounced with clinical recovery. B, Spiked-helmet sign has completely resolved. The QTc interval is within normal range. Also note the absence of Q waves or T-wave inversion that would be indicative of ECG evolution after ischemic ST-segment elevation.

    Given its relatively recent description, SHS remains limited to case reports and small series.1,2 Its true prevalence in the critical care setting is unknown. SHS is usually recognized retrospectively and is associated with a high in-hospital mortality rate.1,2 In the index case series, 6 of the 8 patients died 1 to 10 days after the first ECG recording of SHS (mean, 5.5 days).1,2 Development of this ominous ECG sign in critically ill patients should prompt urgent reassessment. Greater awareness of SHS and its pattern recognition will guide physicians to first consider acute nonischemic pathogenesis.


    Adrian Baranchuk, MD, FACC, FRCPC, FCCS, Professor of Medicine, Clinical Electrophysiology and Pacing, Kingston Health Sciences Centre, Queen’s University, Kingston, K7L 2V7, ONT, Canada. Email


    • 1. Littmann L, Monroe MH. The “spiked helmet” sign: a new electrocardiographic marker of critical illness and high risk of death.Mayo Clin Proc. 2011; 86:1245–1246. doi: 10.4065/mcp.2011.0647CrossrefMedlineGoogle Scholar
    • 2. Simon A, Járai Z. Is the spiked helmet sign the manifestation of long QT syndrome?J Electrocardiol. 2019; 55:16–19. doi: 10.1016/j.jelectrocard.2019.04.011CrossrefMedlineGoogle Scholar
    • 3. Wang K, Asinger RW, Marriott HJ. ST-segment elevation in conditions other than acute myocardial infarction.N Engl J Med. 2003; 349:2128–2135. doi: 10.1056/NEJMra022580CrossrefMedlineGoogle Scholar


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