Neurogenic shock results from loss of sympathetic tone after high cervical or upper thoracic spinal cord injury, particularly above T6¹⁾, leading to hypotension, bradycardia, and impaired reflex cardiovascular control²⁾. However, the failure of thermoregulatory control—specifically, the loss of peripheral vasoconstriction and impaired shivering response—is an equally important but frequently neglected consequence. Temperature regulation in neurogenic shock remains one of the most underexplored aspects of acute spinal cord injury care. A major challenge in managing thermoregulatory dysfunction is the incomplete understanding of disrupted vasomotor and sudomotor control after spinal cord injury³⁾. While hemodynamic instability is often the focus of clinical attention, the accompanying disturbances in thermoregulation may significantly worsen outcomes by aggravating cardiovascular depression, coagulopathy, and metabolic dysfunction^4-8). We propose the Thermal Map Protocol, a novel bedside framework designed to characterize and manage temperature gradients in neurogenic shock through structured thermal assessment and pattern-based intervention.

The specific innovation of this work lies in the development of a pragmatic, four-point ΔT-driven bedside algorithm that operationalizes thermal gradients into actionable Type A/B/C patterns. While thermography and surface temperature monitoring have been previously described across burn care, vascular medicine, and postoperative monitoring, no prior work has proposed a structured, pattern-based framework tailored to neurogenic shock. Recent literature typically focuses on descriptive thermal abnormalities as compared to a clinically adaptable protocol. The Thermal Map Protocol in neurogenic shock focuses on ΔT thresholds, regional mapping zones, and intervention pathways. This framework aims to bridge physiological understanding with structured bedside assessment.

Temperature dysregulation is defined as the inability to maintain core body temperature within the normal range without signs of illness or infection⁹⁾. Following spinal cord injury, particularly above T6, this mechanism of coordination is lost, and injuries at this level are often associated with temperature fluctuations, hypothermia, and hyperthermia^10,11). The body’s capacity to redirect blood flow, conserve heat, or induce sweating becomes regionally impaired below the level of the lesion¹²⁾. Thermoregulation refers to the ability to maintain core body temperature within a narrow range, even when exposed to various environmental temperature challenges¹¹⁾. Under normal physiological conditions, thermoregulation depends on a tightly coordinated interplay between the hypothalamic centers, sympathetic vasomotor control, and cutaneous thermoeffectors⁷⁾. Core temperature regulation is mediated by the preoptic area of the anterior hypothalamus, which integrates peripheral thermal afferent input¹³⁾. The hypothalamus regulates sympathetic functions through descending pathways that synapse in the intermediolateral column of T1-L2 segments of the spinal cord. Noradrenergic and cholinergic efferents from the hypothalamus control vasomotor responses, sudomotor (sweating) function, shivering, and piloerection¹³⁾.

Interruption of descending sympathetic pathways causes cutaneous vasodilation below the level of injury, leading to passive heat loss, impaired shivering thermogenesis, altered sweating responses, and redistribution of blood flow. These changes produce a characteristic temperature asymmetry between the upper and lower body¹⁴⁾. This produces a paradoxical presentation in which patients may appear warm peripherally despite a declining core temperature, potentially misleading early clinical assessment¹⁵⁾. Clinical observations indicate that patients with high spinal cord injuries often experience progressive hypothermia despite adequate ambient temperature¹⁴⁾. This thermoregulatory failure may precipitate bradyarrhythmias, cardiac arrest, and prolonged recovery times¹⁵⁾. Nevertheless, systematic approaches to identify, classify, and manage temperature dysregulation remain lacking in standard neurocritical care protocols. These physiological derangements generate distinct regional temperature patterns that can carry diagnostic and prognostic value¹⁴⁾. In the absence of a structured method to assess these variations, clinicians may rely solely on single-point temperature readings, missing early clues of autonomic instability.

Modern monitoring technologies, such as infrared thermography, digital skin sensors, and wearable temperature patches, offer real-time visualization of skin surface temperatures. Integrating these tools into neurocritical care could permit continuous thermal mapping, allowing early detection of dysautonomic deterioration. Clinically, infrared thermography has demonstrated sensitivity to microvascular changes and has been applied in burn, vascular, and reconstructive surgery⁹⁾. Translating these techniques into spinal injury care may enable clinicians to visualize “thermal territories”—zones of differential perfusion that evolve dynamically as spinal shock progresses or resolves. Furthermore, artificial intelligence-driven thermal analytics could automatically calculate ΔT gradients, generate predictive models, and alert providers to evolving hypothermia or vasomotor instability. Complementarily, this aligns with the growing paradigm of precision neurocritical care, where data-driven pattern recognition supplements traditional bedside evaluation.

We propose the Thermal Map Protocol as an operational bedside tool to guide both diagnosis and management. Its purpose is to convert qualitative temperature impressions (“the patient feels warm”) into quantitative thermal gradients and actionable clinical decisions (Table 1). By converting subjective assessment into measurable data, this approach allows clinicians to generate a ‘thermal fingerprint’ that may reflect injury level and autonomic disturbance.

To improve reproducibility, the Thermal Map Protocol requires standardized definitions of how and where temperature measurements are obtained. We propose using four fixed anatomical sites: (1) forehead as a practical core surrogate, while acknowledging its limitations in vasodilatory states and its susceptibility to ambient influence⁹⁾; (2) supraclavicular region to represent upper-body sympathetic integrity; (3) anterior thigh; and (4) distal lower limb as the most sensitive marker of peripheral vasomotor collapse. All readings should be taken after 2 minutes of skin exposure to room air, with the probe perpendicular to the surface to minimize artifact¹⁶⁾. Provisional, hypothesis-generating ΔT thresholds include: Type A (global hypothermia) defined by <–1.5°C upper–lower body gradient; Type B (segmental sympathetic failure) defined by >2.0°C gradient with preserved warmth above the lesion but cooling below; and Type C (patchy patterns) indicated by >1.0°C variability between adjacent mapped zones. Because true patchiness may mimic artefact, clinicians should confirm findings by repeating measurements, eliminating confounders such as warmers, airflow, or uneven bedding, and verifying consistent probe contact¹⁷⁾. These thresholds are preliminary and require validation; if such operational specificity is not acceptable, the model may be more accurately described as a conceptual ‘framework’ rather than a fully developed protocol.”

Temperature management in neurogenic shock must strike a balance between two competing goals: preventing hypothermia and avoiding excessive rewarming. The Thermal Map Protocol provides guidance for targeted interventions:

● For Type A patterns, systemic hypothermia predominates. Passive rewarming using ambient control and warming blankets is usually sufficient.

● For Type B patterns, active core warming (e.g., forced-air systems, warmed intravenous fluids) is prioritized to prevent afterdrop and maintain cardiac stability.

● For Type C patterns, observation with frequent reassessment helps identify transition phases, as spontaneous reactivation of sympathetic tone can modify perfusion zones.

Furthermore, temperature mapping could help differentiate neurogenic shock from other forms of distributive shock, such as sepsis, where inflammatory hyperthermia predominates. Obtaining a well-defined thermal assessment might support diagnostic accuracy in complex polytrauma or mixed-shock states. In resource-limited environments, temperature dysregulation in spinal cord injury may go undetected due to a lack of continuous monitoring equipment. The Thermal Map Protocol can be adapted using low-cost digital thermometers and manual charting of temperature sites, enabling early recognition even in rural or prehospital settings. Notably, from an educational perspective, the Thermal Map Protocol can be incorporated into simulation-based teaching for emergency and critical care trainees. Simulation scenarios using mannequins with heat-mapped overlays could illustrate the interplay between autonomic pathways, thermoregulation, and hemodynamic responses. Of particular relevance is that the hands-on learning model reinforces theoretical neurophysiology, improving clinicians’ capacity to recognize atypical shock presentations. It also underscores the importance of multisystem thinking—moving beyond hemodynamic parameters to include thermal physiology as a dynamic vital sign.

It is important to emphasize that the associations described between thermal gradients, autonomic dysfunction, and clinical outcomes are extrapolated from broader critical care and sepsis literature rather than derived from studies of this protocol itself. The Thermal Map Protocol should be regarded as an unvalidated, hypothesis-generating framework in comparison to an outcome-proven intervention. Structured thermal assessment may generate physiologic insights and guide future research, but definitive conclusions regarding prognostic value or clinical impact cannot yet be drawn. A prospective validation study—ideally enrolling acute spinal cord injury patients early after presentation, applying standardized thermal mapping at predefined intervals, correlating ΔT patterns with injury characteristics and hemodynamic endpoints, and evaluating responsiveness to targeted interventions—would be required to test its utility. Until such data are available, the protocol may best be described as a conceptual framework that may offer a foundation to guide future studies rather than a strategy expected to improve outcomes at present.

Temperature regulation is not a passive consequence of neurogenic shock—it is an integral reflection of autonomic failure. Recognizing thermal patterns in neurogenic shock may provide additional insight into underlying autonomic physiology. The Thermal Map Protocol offers a new lens through which clinicians can interpret thermal gradients, guide tailored rewarming, and anticipate hemodynamic shifts. This conceptual model bridges the gap between pathophysiology and practice, offering a platform for innovation in monitoring, education, and precision care. Multicentre collaborations will be required to test, validate, and refine this framework and to clarify its potential role in future temperature management strategies for spinal cord injury and neurogenic shock.