Post Your Cases > Legless to legging it: Lipid rescue in ethanol excess?

An 18 yr old male was brought to A&E with a GCS of 3/15 after having collapsed following ejection from a local nightclub. His girlfriend reports he was behaving 'strangely' shortly before bouncers physically removed him from the club. He reportedly complained of chest pain and then collapsed. On arrival in A&E he was tolerating a nasopharyngeal airway, had no gag reflex on pharyngeal suction and had no response even to deeply painful stimuli. His observations were entirely within normal range, as was his arterial blood gas, save for an elevated PO2 due to oxygen therapy, and COHb, likely due to smoking cigarettes. His girlfriend stated that he was drinking beer and shots, but 'no more than usual', and denied any recreational drug use. He had a Reveal (implantable loop recorder) device in situ to investigate arrhythmia, but no further information was known. Additionally, he had a previous A&E attendance 2 months prior for a similar episode of collapse which was not apparently followed up further.
Given the history, and low GCS, the differential diagnosis was either toxic/metabolic or a cerebral cause for his current state. Gold standard of care in our hospital would have been formal securing of the airway, and imaging of the brain with CT, followed by ventilation on ITU overnight if the scan was normal. Unfortunately, the CT scanner was out of service, and the closest facility was over 20 miles away. Additionally, neither our hospital nor the one with a scanner had any ITU beds available.
It was decided that balancing the risk of intubation and transfer versus attempts to improve the patients GCS, the weight was towards the latter. One anaesthetist remained at the patient's head end throughout while a second prepared to attempt reversal of potential toxic agents. 500 mcg of Flumazenil was trialled with no effect. After this, 15 ml/kg of Lipid Rescue was administered, followed by approximately 0.5 ml/kg/min infusion via a peripheral vein. Within 10 min of administration of the bolus, the patient no longer tolerated oral suctioning. A few moments later, without prompting he opened his eyes and began to obey commands. Within 5 further minutes he was sitting up and speaking coherently.
Urine toxicology returned as negative for opiates, benzodiazepines, cocaine and marijuana. Blood alcohol was reported as 271 mg/dl, with the sample drawn more than one hour after the last known ingestion of alcohol.
The ITU team departed A&E, and returned later to find that the patient had absconded by outrunning hospital security; less than 60 min after being completely unresponsive. He had reported to the nurses that he had consumed 15 pints, plus a number of shots prior to his collapse and denied other recreational drugs.

While the blood alcohol level of 271 mg/dl is high, it may not entirely explain the loss of consciousness in a regular drinker. It is possible that that the patient has a seizure disorder which on this occasion and the one 2 months previously was triggered by alcohol (his blood level was only 151 mg/dl previously, from which he awoke spontaneously). Collapse from a primary cardiac cause, such as arrhythmia is possible, although unlikely given the normal chemistry and duration of unconsciousness. Alternatively, the patient may have consumed other short acting recreational drugs which were not picked up on the urine toxicology screen (i.e. ketamine, GHB, GBL, nafyrone, etc.)
Whether purely ethanol related or from a cocktail of substances, the very short time from administration to full alertness is remarkable.
The are clearly many issues over the safe and appropriate use of Intralipid in this case. Some will (rightly) argue that the patient should have been intubated immediately and had a head CT regardless of the logistical considerations. Fortunately, on this occasion that patient has had a positive outcome, and additionally averted having an unnecessary CT, an intubation with a full stomach, an ambulance transfer and an overnight stay on ITU.
Should Intralipid become a standard intervention for low GCS patients to avoid intubation provided an appropriately trained clinician is able to continuously supervise the airway? Perhaps? Perhaps not.
Nonetheless, the author feels there is merit in sharing the details of this case with others and is happy to be contacted with comments.
Wow, Pete. What a great case....I have that image in my mind of a patient running down the hall with iv and ng tube flapping. In some ways, excluding the dramatic exit, the case is reminiscent of Drs. Uncle and Finn's quetiapine case in that lipid administration improved GCS and obviated both intubation and ICU stay. While intubating the trachea generally makes sense to protect the airway in an obtunded patient, there is always potential harm in the unskillfully managed airway (including errant intubation attempts).
Mainly, I think you've opened up the question of using lipid in the patient with mixed or unknown intoxicants and this is a good starting point for the discussion of risk-benefit for lipid infusion in this situation.
BTW, I assume the bolus dose was 1.5mL/kg (15 would be alot!).
Finally, Pete, I wonder if you might consider writing this up.
Guy
September 27, 2010 | Registered Commenter[Guy Weinberg]