The Disrupted Brain

What trickery the brain. Today’s column considers the phenomenon of misbehaving hemodynamics in the multiply injured patient; the cardiovascular gymnastics we can see in blunt trauma when that most mercurial of organs, the brain, is involved.

Trauma management, for good reason, lends itself to the algorithmic; where decisions about complex patients must be made both swiftly and decisively. Most of us grew up with ATLS principles, the ersatz bible of trauma management, and on the whole, the tenets and axioms have held up well, providing foundational understanding of patients who bleed, bleed, bleed.

We know that haemorrhage still accounts for over 50% of deaths from trauma patients, despite the enormous advances made over the past few decades in diagnostics and damage control resuscitation. We know that the causes of hypotension in the trauma patient are 1. Hypovolemia 2. Hypovolemia 3. Hypovolemia 4. Hypovolemia and 5. Other. We have heard, and we have taught, down through the ages, that head injury is not a cause for hypotension. Which is entirely, up to a point, true. But sometimes it is not.

At the best of times, keeping abreast of the hemodynamic response to traumatic haemorrhage in the fresh few minutes is challenging, particularly in the transient responders who continue to haemorrhage; those who need the tap inside turned off by definitive surgical or radiological management. Adding a head injury to the mix, however, significantly adds to the complexity when assessing these patients.

There are the known, macroscopic causes of haemodynamic alteration in neurological injury. Hemorrhage from undiagnosed scalp injury, hypotension from high spinal injury, and, on the flipside, hypertension as part of the Cushing’s reflex.

But it’s the molecular influences, those sequelae unseen, that begin to make the picture complicated. You’ve all seen it; the multiply injured patient whose onscreen numbers look like, as we like to say down under, a dog’s breakfast. Wild systolic blood pressure swings, see-sawing heart rates, other wobbly parameters way out of keeping with the volume changes, the response to loss and replacement, that should make sense.

Animal models and early human blood sampling after head injury reveal a firestorm of mediators which are released immediately after significant brain trauma. Among these are a swathe of cytokines and signalling molecules, as well as the more widely known sympatho-adrenal outpouring. These molecules and messengers have rapidly multiplying downstream effects, sparking off pathological cascades and end-organ disruption, to coagulation and endothelium, hormonal axes, the blood-brain barrier, causing neuro-endocrine responses, to only mention a few. Many of these we see in the moderate to long-term, however it is the effect in the first minutes to hours that we are concerned with here, those manifesting before the CT scan, the invasive monitoring, the printouts of results. In a complex system of haemorrhage and response, we experience the added complexity of the neuro-humoral outpouring.

The emergence of possible biomarkers among this soup remains an exciting area to watch

The molecular details are beyond what we can and should explore in this column. The point, however, is understanding the disconnect between the complexity of the circulating storm occurring in the early phase of the head injured patient, and the simple information we have before us while we make decisions about our trauma patients. This is important primarily as it will influence our decisions about volume resuscitation.

Yes, hypotension is (almost) never caused by head injury alone, but head injury can modulate the presentation of hemorrhagic shock in a myriad ways.