Increased intracranial Pressures following Traumatic Brain Injury in Small Animals
Traumatic brain injury (TBI) results most commonly from motor vehicle accidents and crush injury in dogs and cats, respectively. There are two types of injury:
1) The injury that occurred at the time of impact, termed primary injury, cannot be altered by a practitioner. Examples of primary injuries include skull fractures and soft tissue lacerations.
2) Injury occurring minutes to days after the primary injury, and is called secondary injury. Secondary injury affects intracranial soft tissues, and results in edema, hemorrhage and possible secondary neuronal injury.1
Following TBI local vascular disruption can cause hemorrhage, which sets off a sequence of iron deposition, free radical formation, neuronal membrane damage and edema. Hemorrhage can occur epidural, subdural, subarachnoid, parenchymal and occasionally intraventricular. The Monro-Kellie doctrine states that because the skull is not compressible, the volume is fixed. 2 Therefore, the tissues and fluids that fill this fixed space operate in a state of equilibrium of pressure and volume. If one constituent increases (ex: blood) others must compensate and decrease in volume. Following TBI, edema and hemorrhage add volume to the intracranial space and contribute to intracranial pressure (ICP). As ICP increases, cerebrospinal fluid and blood will be preferentially shunted out of the skull. If ICP continues to increase eventually brain parenchyma will shift out of the skull, resulting in brain herniation.
Early intervention can result in a better long-term outcome for the patient. Changes in ICP can be estimated safely, easily and non-invasively by assessing blood pressure and heart rate together with the neurologic examination. Although others also identified this relationship, in 1902 Harvey Cushing is credited with describing the mathematical relationship between cerebral perfusion pressure (CPP), mean arterial blood pressure (MABP) and intracranial pressure (ICP).4 From this relationship, the following equation was made:
CPP = MABP – ICP.
As ICP increases, MABP must concurrently increase to maintain CPP. (Re-read this part if needed - it is critical!) Systemic baroreceptors recognize this increase as unnecessary for the systemic circulation and therefore the heart rate is slowed. Identification of elevated MABP and bradycardia in the face of decreased mentation is called the Cushing reflex which is a commonly used indicator of increased intracranial pressure in post-traumatic patients.
To recap, what do you need to identify increased ICP in a post traumatic patient??
Right! A stethoscope (or fingers on the pulse), a mean blood pressure measurement and a mini-neuro exam.
Treatment of Elevated ICP
Hyperosmolar medications are the go-to treatments for reducing intracranial pressure. Mannitol, and hypertonic saline are both hyperosmolar medications and both can be used to manage intracranial pressure elevation. Hyperosmolar therapy is suspected to draw fluid from the intraparachymal space into the vascular space, thus reducing intracranial edema. Mannitol has also been shown to be a free radical scavenger, thus helping improve neuronal membrane stability, further inhibiting the development of cytotoxic edema. Unlike mannitol, hypertonic saline can be used for volume resuscitation in the immediate post traumatic period. However, this fluid should not be used long-term for fluid rehydration. Hyperosmolar treatments can be repeated, as needed, throughout the post-traumatic period, however I do not recommend repeating mannitol more than 3 times in 24 hours due to a risk of mannitol accumulation within the brain parenchyma.
Want to talk more about head trauma? Have other neurology related questions? Send me an email or give me a call! I'm here to help.
Please stay safe and healthy during these challenging times.
References
1. Dewey CW. Emergency management of the head trauma patient. Principles and practice. Vet Clin North Am Small Anim Pract. 2000;30(1):207-225. doi:10.1016/S0195-5616(00)50010-2.
2. Witherspoon B, Ashby N. The Use of Mannitol and Hypertonic Saline Therapies in Patients with Elevated Intracranial Pressure: A Review of the Evidence. Nurs Clin North Am. 2017;52:249-260.
3. Kawoos U, McCarron richard M, Auker CR, Chavko M. Advances in Intracranial Pressure Monitoring and Its Significance in Managing Traumatic Brain Injury. Inernational J Mol Sci. 2015;16(12):28979-28997.
4. Fodstad H, Kelly PJ, Buchfelder M. History of Cushing Reflex. Neurosurgery. 2006;59(5):1132-1137.