Older studies in monkeys suggesting the brain could survive about 6 hours of hypoglycaemia created a false sense of security, particularly in the face of clinical experience showing that most patients presenting unconscious to emergency units do wake up. Not all do, and this is usually ascribed to prolonged hypoglycaemia (many hours) prior to reaching hospital. Despite using astrocyte glycogen reserves, and switching to lactate and pyruvate energy sources, 15 minutes of profound hypoglycaemia is probably long enough to inflict some degree of permanent neurological injury, often only detected by more careful cognitive testing than ‘ oh, she is awake now’.1
Getting glucose into the brain.
Active transport of glucose across the blood brain barrier involves active glucose transport by GLUT1 and SGLT2 (GLUT3 gets it into neurons), but getting the glucose into the serum is the first step.2
Oral absorption
The short answer to what foods can be used by the body to raise blood glucose is almost anything, but the detail does matter. Glucose and sucrose, whether oral or buccal, do the trick well, with orange juice and milk being less effective, but the differences are small, and probably not that important in a patient who is symptomatic but conscious. Options include:
- Glucose tablets
- Glucose solution
- Sugar cubes to chew
- Sweets to chew or suck
- More complex (mixed shorter acting and intermediate acting glucose sources)
Intravenous solutions
Getting venous access is often the main issue in a patient with major catecholamine output and vasoconstriction; it is important not to shift task focus from ‘get glucose to the brain’ to the sub-task of ‘put up a drip’. In an unconscious patient, waiting for sugar absoprtion via a hurriedly inserted nasogastric tube of uncertain position is also not sensible, and a more useful step is probably to secure rapid central vein access (e.g. femoral) even if it is only for long enough to get some glucose into the patient’s system; once the catecholamines wear off, finding a peripheral vein will be easier.
There is little evidence that 50% dextrose is better than 10%, but it is routinely the fluid of choice; give enough to raise the serum glucose to within normal range (check this with a glucometer, don’t just assume you have given sufficient.)3. There are 5 g of glucose in 50 ml of 10% dextrose or 10 ml of 50% dextrose (and 5 g in 25 ml of 20%). The Moore and Woollard study gave aliquots of 5 g every minute until there was a clinical response, which usually happened within 8 minutes, and they ended up giving on average 10 g of dextrose to the 10% group and 25 g to the 50% group. Only 51 patients overall, but all woke up with 8% in the former group versus 4% in the latter having a post-treatment GCS <15 (2/25 vs 1/26…)
Arturo Martínez-Piña, D., Alexis Alvarado-Fernández, G., González-Guevara, E., Castillo-Pérez, C., Romero-Luna, G., & Alejandro Torres-Ríos, J. (2022). Hypoglycemia and Brain: The Effect of Energy Loss on Neurons. IntechOpen. doi: 10.5772/intechopen.104210 ↩
Cryer PE. Hypoglycemia, functional brain failure, and brain death. J Clin Invest. 2007 Apr;117(4):868-70. doi: 10.1172/JCI31669. PMID: 17404614; PMCID: PMC1838950. ↩
Moore C, Woollard M. Dextrose 10% or 50% in the treatment of hypoglycaemia out of hospital? A randomised controlled trial. Emerg Med J. 2005 Jul;22(7):512-5. doi: 10.1136/emj.2004.020693. PMID: 15983093; PMCID: PMC1726850. ↩