Abstract
Background
The ‘spiked helmet’ sign is a rare electrocardiographic (ECG) phenomenon characterized by transient ST-segment elevations mimicking an acute coronary syndrome, typically seen in critically ill patients. While often associated with severe physiological stress, its presence in sepsis is particularly uncommon.
Case Presentation
A 68-year-old male with a history of hypertension and diabetes mellitus presented to the emergency department with fever, altered mental status, and hypotension. Initial workup revealed severe sepsis secondary to pneumonia. His ECG showed pronounced ST-segment elevations in leads II, III, and aVF, with a distinctive ‘spiked helmet’ pattern. Troponin levels were mildly elevated, raising concerns for concurrent myocardial ischemia. However, the patient denied chest pain, and further cardiac evaluation, including echocardiography, showed no evidence of ischemia or infarction. Intensive care management included broad-spectrum antibiotics, intravenous fluids, and vasopressors. Despite the severity of his illness, the patient’s condition gradually improved, and repeat ECGs showed resolution of the ST-segment elevations. The ‘spiked helmet’ sign was attributed to severe sepsis-induced autonomic dysfunction rather than primary cardiac pathology.
Conclusion
This case highlights the importance of recognizing the ‘spiked helmet’ sign as a marker of severe stress in critically ill patients, which may mimic myocardial ischemia on ECG. Prompt differentiation between this sign and true ischemia is crucial to avoid unnecessary interventions and focus on managing the underlying critical illness.
Keywords: spiked helmet sign, ECG, severe sepsis, ST-segment elevation, critical illness, myocardial ischemia
Introduction
Electrocardiography (ECG) is a critical tool in the diagnosis and management of acute cardiac conditions. However, certain ECG patterns can mimic life-threatening conditions without underlying cardiac pathology [1]. One such pattern, the ‘spiked helmet’ sign, is an uncommon finding characterized by transient ST-segment elevations that resemble the contour of a spiked helmet. This sign has been primarily reported in critically ill patients with conditions such as respiratory failure, intracranial hemorrhage, and extreme physiological stress [2].
The spiked helmet sign is thought to result from severe autonomic nervous system dysregulation, often in the context of profound systemic illness. Although its presence is a marker of severe underlying disease, it is not commonly associated with sepsis [3]. The differential diagnosis includes acute coronary syndrome (ACS), making recognition of this sign crucial to avoid unnecessary interventions [4, 5].
In this report, we describe the case of a critically ill patient with severe sepsis who exhibited the spiked helmet sign on ECG. This case underscores the importance of distinguishing this unique ECG pattern from true myocardial ischemia, particularly in patients with complex critical illness, to guide appropriate management and improve outcomes.
Case presentation
A 68-year-old male with a history of hypertension, type 2 diabetes mellitus, and chronic obstructive pulmonary disease (COPD) presented to the emergency department with a 3-day history of fever, productive cough, and altered mental status. On examination, the patient was febrile (39.2°C), hypotensive (BP: 80/50 mmHg), tachycardic (HR: 120 bpm), and tachypneic (RR: 28 breaths/min) with an oxygen saturation of 85% on room air. The patient was lethargic and unresponsive to verbal commands.
Initial laboratory investigations revealed leukocytosis (WBC: 18000/μL; Normal range 4500 to 11 000 cells per microliter (μL)), elevated C-reactive protein (CRP: 150 mg/L; normal < 5 mg/L), procalcitonin (10 ng/mL; normal < 0.1 ng/mL), lactate (4.5 mmol/L; normal 0.5–2.2 mmol/L), and mild troponin elevation (0.35 ng/mL; normal < 0.04 ng/mL).
The initial ECG (Fig. 1A) revealed sinus tachycardia with striking ST-segment elevations in leads II, III, and aVF, along with a distinctive spiked helmet sign pattern. Given the patient’s hemodynamic instability and the ECG findings, an acute coronary syndrome was initially suspected. However, the absence of chest pain and the clinical context of sepsis prompted further evaluation. A follow-up ECG (Fig. 1B) obtained after clinical stabilization demonstrated resolution of the ST-segment elevations and disappearance of the spiked helmet sign.
Figure 1.
(A) Initial ECG on admission showing sinus tachycardia and ST-segment elevations in leads II, III, and aVF with a characteristic spiked helmet pattern. (B) Repeat ECG after 72 h showing resolution of ST-segment elevations.
Echocardiography showed preserved left ventricular function without wall motion abnormalities or signs of ischemia. Given the lack of definitive evidence of myocardial infarction and the severe sepsis diagnosis, the patient was managed in the intensive care unit (ICU) with broad-spectrum antibiotics, intravenous fluids, and vasopressors.
Over the next 72 h, the patient’s condition stabilized, with improvement in blood pressure and mental status. Repeat ECGs showed resolution of the ST-segment elevations, and the spiked helmet sign disappeared. The patient was gradually weaned off vasopressors, and his antibiotic regimen was narrowed based on culture results. He continued to improve and was eventually transferred to the general medical ward. The spiked helmet sign was attributed to sepsis-induced autonomic dysregulation rather than primary cardiac pathology.
Discussion
The spiked helmet sign is an uncommon but important ECG finding that is typically associated with extreme physiological stress in critically ill patients [6]. This sign, characterized by a sharp upsloping ST-segment elevation resembling a spiked helmet, can easily be mistaken for an acute myocardial infarction, leading to unnecessary and potentially harmful interventions [5, 7].
In this case, the presence of the spiked helmet sign in a patient with severe sepsis highlights the importance of considering non-cardiac causes of ST-segment elevation, particularly in the context of critical illness [5]. The pathophysiology behind the spiked helmet sign is thought to involve severe autonomic nervous system dysregulation, possibly exacerbated by factors such as hypoxia, acidosis, and systemic inflammation—all of which were present in this patient [6].
While the exact mechanism remains unclear, it is crucial for clinicians to recognize this pattern and differentiate it from true ischemic changes on ECG. Management should focus on treating the underlying systemic illness rather than initiating unwarranted cardiac interventions [7]. This case also underscores the value of a thorough clinical evaluation and the use of adjunctive diagnostic tools, such as echocardiography, to guide appropriate management.
Conclusion
The spiked helmet sign is a rare but significant ECG finding in critically ill patients, particularly those with severe sepsis. Recognizing this sign is essential to prevent misdiagnosis of acute coronary syndrome and to ensure appropriate management of the underlying critical illness. This case emphasizes the importance of a comprehensive approach to interpreting ECG findings in the context of the patient’s overall clinical picture. By focusing on treating the systemic cause of the ECG changes, clinicians can improve patient outcomes and avoid unnecessary interventions.
Contributor Information
Hashim Manea, Vascular Surgery Department, Oregon Health and Science University, 110 N Tomahawk island Dr, Portland, OR, 97217, United States; University of Warith Al-Anbiyaa, College of Medicine, Oun street, Karbala, 10072 Iraq; Department of Clinical Research, University of Jamestown, Nassiryah, Thi Qar, 64001, Jamestown, ND, United States.
Ahmed Qasim Mohammed Alhatemi, Department of Internal Medicine, Al Nasiriyah Teaching Hospital, Nassiryah, Thi Qar, 64001, Iraq.
Mohammedbaqer Ali Al-Ghuraibawi, University of Warith Al-Anbiyaa, College of Medicine, Oun street, Karbala, 10072 Iraq.
Ghaith Asaad Alhumairi, Royal Shrewsbury Hospital, Mytton Oak Road, Shrewsbury, SY3 8XQ, United Kingdom.
Ali Saad Al-Shammari, College of Medicine, university of Baghdad, Nahdha, Baghdad, 10048, Iraq.
Abdullah Muataz Taha Al-Ibraheem, Al-Kindy College of Medicine, university of Baghdad, Nahdha, Baghdad, 10048, Iraq.
Ibrar Ahmad, Department if Medicine, University of Stavanger, Mail box 8600, 4036 Stavanger, Norway.
Hussein Safaa Abdulammer, Anesthesia Techniques Department, College of Health and Medical Techniques, Al-Mustaqbal University, Babylon 51001, Iraq.
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