In 1973 pt (age 18) was huffing aerosol deodorant (halogenated hydrocarbons) through a filter made of toilet paper. After inhalation of 2 cans, pt became disoriented followed by agitation and collapse. There was cessation of heartbeat & breathing - friends took pt to ER and performed CPR en route 2-3 times. Upon presentation, pt was flat-lined on EKG - successful rescuscitation with closed chest massage and ventilatory support.
Following rescuscitation pt had intermittent decerebrate posturing with no corneal or abdominal reflexes and totally unresponsive except for a pupillary response. Pt admitted to ICU with endotrach in place and remained unresponsive as noted in prior sentence for 18-24 hours. Over the next few days pt remained somewhat unresponsive although at times would cry out (at different times spontaneously cried out - he made me do it, mother, father, names of friends). After 3 weeks pt was transferred to larger hospital for neurological eval. In the days prior to transfer, pt had progressed and was able to sit up in bed and would cry out occasionally. Nasogastric tube remained in place as did catheter.
Upon admit at transfer pt had temp 38 centigrade, bp 130/100. Not alert. Somewhat unresponsive to verbal commands. Quite agitated with excessive restlessness and increased physical activity and crying out episodes. Pt could doll's eye, fundoscopic exam revealed well-defined circumscribed disc margins. Corneal reflex direct and consensual bilaterally. Good pupillary light reflex. Reflexes somewhat diminished in ankles bilaterally. Absent left abdominal reflex. Unsustained clonus bilaterally. No Babinski. Active Hoffman's bilaterally.
During 2 week stay at 2nd hospital SMA 6 was wnl. One SMA 12 value reported SGOT of 141. EKG sinus tachycardia but otherwise wnl. On 2d day of stay nasogastric tube removed and pt gradually started taking pills, fluids and food with encouragement. Persistenly and daily pt had crying out episodes and episodes of extreme emotional lability during which there was a great deal of motor activity. Pt would respond to verbal command and could talk although somewhat incoherently and had a dysarthria. Recent memory poor although past memory fairly well intact. Disoriented at times as far as place. EEG revealed abnormal waves indicative of generalized encephalopathy. Pt revelaed changes consistent with organic mental syndrome secondary to inhalation of halogenated hydrocarbon which caused previous cardiopulmonary arrest and led to anoxic brain damage. Pt discharged to home 31 days post-event in hopes familiar surroundings would aid in adjustment to new condition.
It appears that this pt is a rare survivor of what is now known as "sudden sniffing death". Consequently, I can find very little information regarding outcomes - hence my attempts to determine GCS. I am trying to determine if her estimated GCS was a reliable prognostication of outcome. Any help would be appreciated.
I have many issues with the "Glasgow Coma Scale" particuliarly in the pre-hospital environment. It is now taught in basic EMT classes.
Evaluation of neurological injuries is above the pay scale of a basic level-one EMT, and it delays transport. Not, if, maybe, or possibly. In some systems EMT's are written up for not having "complete" forms filled out to include the Glasgow coma scale. Delay in transport for this examination may be ten minutes, as the EMT calls someone or consults a book "to do it right". The determination of the Glasgow number wastes time in the pre-hospital environment.
At the hospital the EMT evaluation may or may not be utilized. The Glasgow coma numer on the patient chart may be the one produced by a neurologist from eight to twenty-four hours after the injury.
The scale itself was developed "off the top of the head" and only then was it decided to conduct followups to see what kind fo predicative value it had. And what value does it have? To assist in a decision to continue treatment? What exactly is the point in the Glasgow coma scale?
Now I will admit that it might be a good idea to use operational research techniques to come up with some sort of a predicative system. How about the delphic system,, where six physicians take a guess based upon their experience as to the chances for recovery? I don't suggest that to be facetious.
Incidentally, in your patient presentation you state "friends took to ER and there was cesation of heart and breathing and they performed CPR "three times". In a moving car? I find this acount to be less than credible. This, of course is not your fault. As for being flat-lines and being resuscitated with CPR I have never seen this happen. Only if the flat-line is coarsened with epinephrine and then a defribrilation is performed is there generally a good outcome. It may be possible, but I have never seen flatlone converted to a rhythym compatable with life solely with CPR. Was there ALS intervention? There are lots of missing pieces in the history.
Thank you for your responses. Unfortunately, the only information I have is the 1973 records from the second hospital where pt was transferred 20 days after the event. Their information presumably came from records at the initial hospital and from the referring physician. The information from the hospital at which pt first presented is not available - those records were destroyed years ago and the tertiary hospital (2nd hospital) only had discharge summary and EEG reports from which the information presented above was gleaned.
Any other thoughts on prognostication from the available information?
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