Pupillary evaluation for differential diagnosis of coma

Abstract

Objectives: To determine the usefulness of bedside evaluation of pupils in determining the aetiology of coma by adopting a probabilistic approach. Patients and methods: One hundred and fifteen consecutive patients presenting with coma were enrolled in this prospective cohort during the 12 month study period in the emergency room of a community teaching hospital. Patients underwent structured clinical examinations and laboratory and imaging tests. Assignment of aetiology of coma was based on strict adherence to predetermined criteria and achieved by consensus of the two physician investigators. One year follow up was obtained in all patients. Results: Aetiology of coma was determined in 98% of the patients. It was metabolic in 69 patients (60%) and structural in 46 patients (40%). Metabolic causes included drug overdose, acute alcohol intoxication, hypoglycaemia, sepsis, and pneumonia. Structural causes included intracerebral haemorrhage, subarachnoid haemorrhage, cerebral infarction, subdural haematoma, and epidural haematoma. Multivariate logistic regression analysis showed light reflex loss (likelihood ratio for positive test result 3.59) and anisocoria (likelihood ratio for positive test result 9.0) as independent predictors of structural origin. Conclusions: In this prospective study of patients presenting to the emergency room of a community based teaching hospital with coma, in about 60% the coma is of metabolic origins and in about 40% of structural origins. Light reflex loss and anisocoria suggest a structural aetiology.

Etiology and outcome of medical coma in a tertiary hospital in Northwestern Nigeria

“…[7] Thus, a better understanding of causes and outcome, especially in a resource poor setting, is key to improving the approach and to plan rational management of medical coma. Moreover, since knowledge of disease probability is crucial in terms of differential diagnosis, [8,9] relative frequency of various causes of coma should be investigated in an actual cohort.…”

“…The relative frequency of various causes of coma in our patients was similar to previous report outside Nigeria in spite of the geographic and technological differences. [9][10][11] However, when the etiological factors were considered individually, stroke appeared the most common cause. This finding agrees with the report of Obiako and his colleagues in southwestern Nigeria.…”

Pupillary abnormalities in non-selected critically ill patients: an observational study

“…To the best of our knowledge, no previous study has reported the prevalence of PAs in this population. Our findings should be cautiously compared with those from previous studies that almost uniquely included neurosurgical patients (4)(5)(6)(7)(8)(9). The prevalence of PAs may vary according to the quality of the pupillary evaluation, which can be challenging at the bedside (2,(10)(11)(12)(13)(14).…”

“…The size and reactivity to light of each pupil allows an exploration of brainstem function and should be recorded periodically in intensive care units (ICU) (2)(3)(4). Indeed, pupillary abnormalities (PAs), i.e., anisocoria and/or pupillary areflexia, may represent a sign of acute brain damage, which is particularly informative in comatose patients (1)(2)(3)(4). In neurosurgical patients, PAs are frequent and represent a reliable marker of brain herniation or ischemia (5)(6)(7)(8).…”

Alteración del estado de conciencia en el paciente intoxicado

“…La caracterís-tica diferencial de un coma tóxico es la disociación de los hallazgos físicos esperados, por ejemplo, un reflejo pupilar a la luz intacto en ausencia de respuesta oculovestibular y motora 19,20 . Este fenómeno de disociación es explicado porque varias funciones del tallo cerebral tienden a ser más vulnerables a la agresión tóxica y metabólica que los reflejos pupilares a la luz 21,22 . Dentro de las excepciones para considerar están la intoxicación por opioides, barbitúricos y amitraz que producen miosis puntiforme no reactiva, mientras que algunos agentes anticolinérgicos causan midriasis no reactiva como en Tabla 2.…”