Suppression of brainstem reflexes in barbiturate coma.

Grattan-Smith, Padraic J.; Butt, Warwick

doi:10.1136/adc.69.1.151

Cited by 26 publications

(12 citation statements)

References 5 publications

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“…Local cutaneous stimulation of the neck activates sympathetic fibers via connections with the ciliospinal center at C8-T2 [ 2 - 4 ]. The induction of a pentobarbital coma is expected to cause a suppression of all brainstem reflexes, which can obscure the clinical signs of neurological deterioration [ 5 - 6 ]. In some cases, the ciliospinal reflex may not be suppressed in a barbiturate coma and can become exaggerated.…”

Section: Discussionmentioning

confidence: 99%

Pitfall in Pupillometry: Exaggerated Ciliospinal Reflex in a Patient in Barbiturate Coma Mimicking a Nonreactive Pupil

Mullaguri

Katyal

Sarwal

et al. 2017

Cureus

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Although a neurological examination is fundamental to the evaluation of comatose patients, it is less reliable in a medically induced coma. A commonly misinterpreted finding in patients in a pentobarbital coma is altered pupillary reactivity secondary to an exaggerated ciliospinal reflex. Recognizing an exaggerated ciliospinal reflex in patients in a pentobarbital coma is important and may prevent unnecessary intervention. We present a patient induced in a pentobarbital coma for the treatment of status epilepticus who exhibited a nonreactive pupil secondary to an exaggerated ciliospinal reflex confirmed by pupillometry. We also discuss the anatomy of the ciliospinal reflex and literature regarding its clinical relevance.

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Section: Discussionmentioning

confidence: 99%

Pitfall in Pupillometry: Exaggerated Ciliospinal Reflex in a Patient in Barbiturate Coma Mimicking a Nonreactive Pupil

Mullaguri

Katyal

Sarwal

et al. 2017

Cureus

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“…12 But these scoring systems are not reliable in some conditions such as locked-in syndrome, 5 hypothermia, 6 or drug intoxication that can lead to misdiagnosis of brain death. [7][8][9] In this regard, over the past decades studies have focused on the use of biomarkers in the prediction of brain death after brain trauma. Our study evaluated the S100B protein in serum as a biomarker in the prediction of brain death after brain trauma.…”

Section: Discussionmentioning

confidence: 99%

“…4 Brain death can be evaluated using certain clinical criteria and by performing confirmatory tests (Table 1). 4 However, misdiagnosis of brain death is possible if a locked-in syndrome, 5 hypothermia 6 or drug intoxication [7][8][9] is not recognized. 4 Although there are scoring and survival probability systems, such as the Glasgow Coma Scale (GCS), for the assessment of injury to the head and other body parts, 10 physiological scoring systems such as the Revised Trauma Score 11 and TRISS methodology (Trauma Scoring And Injury Severity Score) can be used.…”

mentioning

confidence: 99%

S100B Protein Value in Predicting Brain Death After Head Trauma

Shakeri

Ghafari

Panahi

et al. 2014

Neurosurgery Quarterly

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“…En el tratamiento de los pacientes neurocríticos se utilizan habitualmente benzodiacepinas, propofol, opiáceos y barbitúricos que pueden enmascarar la exploración neurológica. Los barbitúricos a dosis elevadas y mantenidas llegan a producir coma profundo sin respuesta a estímulos algésicos, ausencia de reflejos troncoencefálicos y EEG sin actividad bioeléctrica cerebral [12][13][14] . El pentobarbital y el tiopental son barbitúricos de acción corta y ultracorta de efectos similares que se diferencian sólo en su farmacocinética.…”

Section: Ausencia De Fármacos Depresores Del Sistema Nervioso Centralunclassified

Diagnóstico de muerte encefálica

Escudero

2009

Medicina Intensiva

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Brain death has been recognized by the scientific community as the person's death, and accepted in the legislation of different countries. Brain death is defined as the irreversible ending of the functions of all the intracranial neurological structure in both the brain and brain stem. This clinical situation appears when intracranial pressure exceeds the patient's systolic blood pressure, leading to brain circulatory arrest. The most frequent are cerebral hemorrhage and cranioencephalic trauma. Clinical diagnostic must be done by doctors with expertise in neurocritical patient treatment. This diagnosis is based on a systematic, complete and extremely rigorous clinical examination that confirms a non-reactive coma, absence of brain stem reflex, and absence of spontaneous breathing. Instrumental tests may be obligatory in some cases, this depending on each country. Electroencephalogram and evoked potentials are the electrophysiological tests used. In patients treated with sedative drugs, cerebral blood flow evaluation tests, such as cerebral angiography, transcranial Doppler or 99Tc-HMPAO scintigraphy, will be used. More than 92% of the transplants performed in Spain are performed with brain death donor organs. Brain death confirmation is a high responsibility act, with medical, ethical and legal significance since it requires removal of all artificial support, or organs extraction for transplant. Extensive knowledge on its diagnostic and correct decision making avoid unnecessary use of resources and improves management of organs for transplant.

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Suppression of brainstem reflexes in barbiturate coma.

Cited by 26 publications

References 5 publications

Pitfall in Pupillometry: Exaggerated Ciliospinal Reflex in a Patient in Barbiturate Coma Mimicking a Nonreactive Pupil

Pitfall in Pupillometry: Exaggerated Ciliospinal Reflex in a Patient in Barbiturate Coma Mimicking a Nonreactive Pupil

S100B Protein Value in Predicting Brain Death After Head Trauma

Diagnóstico de muerte encefálica

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