Clinical Presentation and Causes of Non-traumatic Spinal Cord Injury: An Observational Study in Emergency Patients.

Introduction: Diagnosing non-traumatic spinal cord injury (NTSCI) is often challenging. However, clear discrimination from non-spinal pathologies, e.g., "myelopathy-mimics" (MMs), is critical in preventing long-term disability and death. In this retrospective study we (1) investigated causes of NTSCI, (2) identified clinical markers associated with NTSCI and (3) discuss implications for NTSCI management. Methods: Our sample consisted of 5.913 consecutive neurological and neurosurgical patients who were treated in our emergency department during a one-year period. Patients with a new or worsened bilateral sensorimotor deficit were defined as possible NTSCI. We then compared clinical and imaging findings and allocated patients into NTSCIs and MMs. Results: Of ninety-three included cases, thirty-six (38.7%) were diagnosed with NTSCI. Fifty-two patients (55.9%) were classified as MMs. In five patients (5.4%) the underlying pathology remained unclear. Predominant causes of NTSCI were spinal metastases (33.3%), inflammatory disorders (22.2%) and degenerative pathologies (19.4%). 58.6% of NTSCI patients required emergency treatment. Presence of a sensory level (p = <0.001) and sphincter dysfunction (p = 0.02) were the only significant discriminators between NTSCI and MMs. Conclusion: In our study, one-third of patients presenting with a new bilateral sensorimotor deficit had NTSCI. Of these, the majority required emergency treatment. Since there is a significant clinical overlap with non-spinal disorders, a standardized diagnostic work-up including routine spinal MRI is recommended for NTSCI management, rather than an approach that is mainly based on clinical findings.

The accuracy of initial diagnoses in coma: an observational study in 835 patients with non-traumatic disorder of consciousness.

BACKGROUND: Management of patients with coma of unknown etiology (CUE) is a major challenge in most emergency departments (EDs). CUE is associated with a high mortality and a wide variety of pathologies that require differential therapies. A suspected diagnosis issued by pre-hospital emergency care providers often drives the first approach to these patients. We aim to determine the accuracy and value of the initial diagnostic hypothesis in patients with CUE. METHODS: Consecutive ED patients presenting with CUE were prospectively enrolled. We obtained the suspected diagnoses or working hypotheses from standardized reports given by prehospital emergency care providers, both paramedics and emergency physicians. Suspected and final diagnoses were classified into I) acute primary brain lesions, II) primary brain pathologies without acute lesions and III) pathologies that affected the brain secondarily. We compared suspected and final diagnosis with percent agreement and Cohen's Kappa including sub-group analyses for paramedics and physicians. Furthermore, we tested the value of suspected and final diagnoses as predictors for mortality with binary logistic regression models. RESULTS: Overall, suspected and final diagnoses matched in 62% of 835 enrolled patients. Cohen's Kappa showed a value of κ = .415 (95% CI .361-.469, p < .005). There was no relevant difference in diagnostic accuracy between paramedics and physicians. Suspected diagnoses did not significantly interact with in-hospital mortality (e.g., suspected class I: OR .982, 95% CI .518-1.836) while final diagnoses interacted strongly (e.g., final class I: OR 5.425, 95% CI 3.409-8.633). CONCLUSION: In cases of CUE, the suspected diagnosis is unreliable, regardless of different pre-hospital care providers' qualifications. It is not an appropriate decision-making tool as it neither sufficiently predicts the final diagnosis nor detects the especially critical comatose patient. To avoid the risk of mistriage and unnecessarily delayed therapy, we advocate for a standardized diagnostic work-up for all CUE patients that should be triggered by the emergency symptom alone and not by any suspected diagnosis.

Causes of brain dysfunction in acute coma: a cohort study of 1027 patients in the emergency department.

BACKGROUND: Coma of unknown etiology (CUE) is a major challenge in emergency medicine. CUE is caused by a wide variety of pathologies that require immediate and targeted treatment. However, there is little empirical data guiding rational and efficient management of CUE. We present a detailed investigation on the causes of CUE in patients presenting to the ED of a university hospital. METHODS: One thousand twenty-seven consecutive ED patients with CUE were enrolled. Applying a retrospective observational study design, we analyzed all clinical, laboratory and imaging findings resulting from a standardized emergency work-up of each patient. Following a predefined protocol, we identified main and accessory coma-explaining pathologies and related these with (i.a.) GCS and in-hospital mortality. RESULTS: On admission, 854 of the 1027 patients presented with persistent CUE. Their main diagnoses were classified into acute primary brain lesions (39%), primary brain pathologies without acute lesions (25%) and pathologies that affected the brain secondarily (36%). In-hospital mortality associated with persistent CUE amounted to 25%. 33% of patients with persistent CUE presented with more than one coma-explaining pathology. In 173 of the 1027 patients, CUE had already resolved on admission. However, these patients showed a spectrum of main diagnoses similar to persistent CUE and a significant in-hospital mortality of 5%. CONCLUSION: The data from our cohort show that the spectrum of conditions underlying CUE is broad and may include a surprisingly high number of coincidences of multiple coma-explaining pathologies. This finding has not been reported so far. Thus, significant pathologies may be masked by initial findings and only appear at the end of the diagnostic work-up. Furthermore, even transient CUE showed a significant mortality, thus rendering GCS cutoffs for selection of high- and low-risk patients questionable. Taken together, our data advocate for a standardized diagnostic work-up that should be triggered by the emergency symptom CUE and not by any suspected diagnosis. This standardized routine should always be completed - even when initial coma-explaining diagnoses may seem evident.

Coma of unknown origin in the emergency department: implementation of an in-house management routine.

BACKGROUND: Coma of unknown origin is an emergency caused by a variety of possibly life-threatening pathologies. Although lethality is high, there are currently no generally accepted management guidelines. METHODS: We implemented a new interdisciplinary standard operating procedure (SOP) for patients presenting with non-traumatic coma of unknown origin. It includes a new in-house triage process, a new alert call, a new composition of the clinical response team and a new management algorithm (altogether termed "coma alarm"). It is triggered by two simple criteria to be checked with out-of-hospital emergency response teams before the patient arrives. A neurologist in collaboration with an internal specialist leads the in-hospital team. Collaboration with anaesthesiology, trauma surgery and neurosurgery is organised along structured pathways that include standardised laboratory tests and imaging. Patients were prospectively enrolled. We calculated response times as well as sensitivity and false positive rates, thus proportions of over- and undertriaged patients, as quality measures for the implementation in the SOP. RESULTS: During 24 months after implementation, we identified 325 eligible patients. Sensitivity was 60 % initially (months 1-4), then fluctuated between 84 and 94 % (months 5-24). Overtriage never exceeded 15 % and undertriage could be kept low at a maximum of 11 % after a learning period. We achieved a median door-to-CT time of 20 minutes. 85 % of patients needed subsequent ICU treatment, 40 % of which required specialised neuro-ICUs. DISCUSSION: Our results indicate that our new simple in-house triage criteria may be sufficient to identify eligible patients before arrival. We aimed at ensuring the fastest possible proceedings given high portions of underlying time-sensitive neurological and medical pathologies while using all available resources as purposefully as possible. CONCLUSIONS: Our SOP may provide an appropriate tool for efficient management of patients with non-traumatic coma. Our results justify the assignment of the initial diagnostic workup to neurologists and internal specialists in collaboration with anaesthesiologists.