What is the physiological response to tonsillar herniation?
Tonsillar herniation or “coning” describes the forced downward motion of the cerebellar tonsils through the foreman magnum resulting in compression of the brain-stem and cervical cord in response to raised intracranial pressure (ICP) .
When intracranial pressure (ICP) exceeds mean arterial pressure (MAP), brain perfusion and thus oxygenation is compromised resulting in sympathetic discharge causing an initial increase in heart rate and MAP. The increased MAP activates the aortic and carotid baroreceptors which causes a reflex bradycardia via the parasympathetic nervous system.
As ICP increases further, the cardio-respiratory centres within the brain-stem become compressed resulting in pathologically irregular respiratory patterns (Cheyne-stokes respirations), widening pulse pressure and bradyarrhythmia. This is collectively referred to as Cushing’s Triad .
During the first night of his Intensive Care stay he developed increasing cardiovascular instability and high volume, dilute urine output. A diagnosis of Diabetes Insipidus was made and successfully treated with 1 microgram boluses of Desmopressin followed by an infusion of Arginine Vasopressin. He was taking spontaneous breaths and was coughing on tracheal suctioning. His intravenous sedation was stopped at this stage to assess neurological function.
At the morning assessment, the bedside nurse noted that he was no longer taking any spontaneous breaths and the cough reflex on deep suctioning was no longer present. Brain-stem death was suspected and plans for formal testing were put in place for later that day.