Low glucose in shunt infections and meningitis: Further comments on the mechanisms behind this phenomenon

With this mid-twentieth century title paraphrasing an interesting article by Petersdorf, Swarner and Garcia, I preface a question that has been bugging me: Why is it that glucose drops in (bacterial) CNS infections? While I’m not 100% sure of the answer, and the question keeps coming back, I feel I can venture some possible explanations:

Bacteria clog up the pipe that connects the blood with the brain. As a result, glucose barely gets through. Drano to the rescue.
It is a laboratory conspiration. They know how to fool you. Furthermore, there will be a massive earthquake next Cinco de Mayo along Route 66, and we all will go straight to hell. Your inner voice is right. Just run the case by your ID partner, he may protect you from them.
Bacteria reach for the brain master switch, turn it on and swallow the key — the “brain hyper-utilization” theory. It’s like going on vacations in the summer and leaving the AC set at 60·. The result: a glucose energetic crisis. If you believe this, you probably also voted for Obama and oppose offshore drilling.
Bacteria are insatiable and primitive. They only want to eat and procreate. And they are millions and counting, so they will get what they want — the “bacterial metabolism” theory. This has more distant roots in your past. Your mom was giving you antibiotics even for a loose tooth.
As bacteria run on sugar, white cells are deployed to the CNS to hide it. The more the white cells, the faster glucose disappears. Because of old resentments, WBCs will kill with a machete any bacterium with a sugar breath. And I mean kill it — for real. Beheaded germs lose the proteins via their severed jugular veins. The result is a mess, and there is no clear winner. The prognosis is guarded. Either you’ve stolen your child’s PlayStation, or you are in bad need for vacations to a remote island.
Bacteria never liked glucose too much. They would do Splenda if they could. White cells, in turn, are picky. They are the ones to blame.

But I truly believed that it was related to a dysfunction in the blood-to-CSF glucose pump. For instance, some genetic mutations of the GLUT1 gene can result in various problems, with CSF hypoglycorrhachia being perhaps the worst. Those kids can benefit from ketogenic diets.

Cancerous cells in vitro have a rapid glycolytic rate compared with normal cells. It would make sense that they would utilize more glucose. However, in a patient with leptomeningeal carcinomatosis presenting with low CSF glucose, IV infusion of the sugar did not increase his CSF levels, suggesting an abnormal blood-to-CSF transport of glucose (Jann S. Ital J Neurol Sci. 1988;9:83-88). But Petersdorf and pals, in their detailed studies in which mongrel dogs were branded with 100 million pneumococci intrathecally, demonstrated that bacteria per se did not reduce CSF glucose, but that this occurred only in the presence of hungry leukocytes (Petersdorf RG. Proc Soc Exp Biol Med. 1960;104:65-68).

It is curious that there is no wide consensus to define low CSF glucose. Some will say less than 50 mg/dL, or 40 mg/dL, or less than half of your serum glucose concentration. If you do a peripheral stick, do you do it before or after? Before — you don’t want the lumbar tap to result in an epinephric, stressed child. How long before? That gets less clear. The lag time for equalization between the CSF space and blood compartment is 0.5 to 4 hours. So obtaining simultaneous peripheral glucose levels may be misleading, but based on correlation studies in fasting individuals, there is agreement in obtaining a level 30 minutes to 1 hour before the tap. And regarding the well-known association with bacterial meningitis, hypoglycorrhachia can also present in patients with metabolic disorders, aseptic meningitis, meningeal carcinomatosis, subarachnoid hemorrhage and primary hypoglycemia.

Despite all this, and from the clinician point of view, it makes more sense to me and to my neurosurgeon colleagues to imagine a bacterium reclined against the posterior ventricular horn, indulging on glucose and pooping proteins. That would explain so much.

Follow the PediatricSuperSite.com on Twitter.