Prehospital management of cerebral herniation

Cerebral herniaton is a process where brain tissue is moved, because of high pressure. The tissue is moved from its origin to another loaction inside the skull, or down through the foramen magnum to the spinal channel. Cerebral herniaton is caused by increased intracranial pressure (ICP) due to volume filling processes, such as intracranial bleeding. Because herniation/ high ICP compresses vital structures and disturbs the natural blood flow, it is a highly lethal process.

Cerebral herniation should be suspected in a head trauma patient with a low, or rapidly falling level of consciousness.  Abnormal extension of the extremities, or no reaction at all can be seen when the patient is subjected to painful stimuli. Often one or both pupils are dilated and not responsive to light as the herniation process compresses one or both of the oculomotor nerves. Because cerebral herniation is caused by increased ICP, the cushing's triad with hypertension, bradycardia and irregular breathing is also often seen. It is important to notice that all of these signs are seen in the late stages of raising ICP, and that absence of these signs does not exclude serous brain injury.

Management of all serious traumatic brain injuries:

•          Secure ABCs to prevent secondary brain damage, which is damage to brain parenchyma due to hypoxia or hypotension. 
•          Secure the vertebral column according to local protocol.
•          Consider elevating the head end of the gurney about 30 degrees, this provides the optimal position to prevent further rise in ICP, because of increased venous return without compromising arterial flow to much.
•           Quickly and safely transport the patient to the closest appropriated trauma facility with neurosurgery, consider using air transport. Alert the trauma team well in advance.
• Closely monitor and document vital signs and level of consciousness.                                                            

Management of the herniating patient:

•           Mild hyperventilation of the patient. This lowers the partial pressure of CO₂ in the parents’ blood, which will constrict cerebral vessels. The vasoconstriction decreases the volume occupied by blood vessels within the skull and reduces filtration of plasma over the capillaries, both lowering the ICP. It is important to not ventilate the patient too aggressively, as this will wash out too much CO₂ , constricting the cerebral vessels to levels leading to ischemia. To the adult patient, hyperventilation should be administered as 20 ventilations per minute, with normal tidal volumes. To avoid ischemia hyperventilation should be monitored with capnometry or capnography, and EtCO₂ be kept at levels from 30-35 mmHg or about 4,0-4,5 kPa. To avoid cerebral ischemia hyperventilation should not be used as a profilactic treatment, but only used in patients with suspected ongoing herniation. The hyperventilation should be discontinued when if the signs of herniation resolve.                                           
•           Consider administrating a hypertonic solution IV, such as hypertonic NaCl or Mannitol if the transport time is intermediate or long. This will remove fluid from the brain due to the higher osmolality of the blood after such infusion. It is widely in use in the intrahospital setting, but there is some controversy to its use in the prehospital setting.  

Sources:

http://www.braintrauma.org/pdf/protected/Prehospital_Guidelines_2nd_Edition.pdf

http://tidsskriftet.no/article/1707571/

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Understanding the Cushing's Triad

The Cushing`s Triad is a triad of three signs, which is typically seen in the late stages of patients with elevated intracranial pressure (ICP). Both the sympathetic and parasympathetic nervous system plays important roles in the triad, which consists of:

• Hypertension (increased blood pressure)
• Bradycadria (decreased heart rate)
• Irregular breathing pattern

Why hypertension?

When there is an elevated ICP due to for example intracranial bleeding or edema, cerebral vasculature will be increasingly compressed with rising ICP, leading to cerebral ischemia. To combat this the sympathetic nervous system is activated. The increased sympathetic tone will primary constrict the arterioles of the body, mediated by alpha 1 adrenergic receptors. Since our mean arterial blood pressure (MABP) is the product of cardiac output (CO) and systemic vascular resistance (SVR), the MABP will rise, in other words, the patient will develop hypertension. An increased pulse pressure (difference between systolic and diastolic blood pressure) is also seen, because primary the systolic blood pressure rises, whereas the diastolic pressure remains the same. The cerebral vessels are not affected by this vasoconstriction, protecting the brain form ischemia.

The hypertension seen in patients with increased ICP is part of the cerebral autoregulation, trying to keep cerebral perfusion pressure (CPP) relatively constant, even though the ICP increases. CPP is the difference between MABP and ICP (CPP=MABP-ICP), so increasing MABP by contracting arterioles makes sense when the ICP is elevated. The brain also shunts away cerebrospinal fluid in order the combat the rising ICP. If these and other compensatory mechanisms are inadequate, ICP will continue to rise, reducing CPP to levels leading to global ischemia of brain tissue. When ICP equals MABP, the CPP will be 0, and there will be no circulation to the brain, a state known as brain tamponade. 

Why bradycardia?

The initial sympathetic tone will initially cause tachycardia, and increased contractility of the heart mediated primarily by beta 2 adrenoreceptors. This will increase cardiac output, and thus increasing MABP together with the increased systemic vascular resistance. The increased MABP will stretch and activate the high pressure baroreceptors in the aortic arch and carotid sinus, which via the vagus and glossopharyngeal nerve respectably, will signal that there is and increased MABP to the cardiovascular control center in medulla oblongata. When there is an elevated MABP sympathetic tone will be reduced and parasympathetic tone will be increased, leading to bradycardia. The signal to the arterioles to constrict, due to the high ICP, remains leaving the patient with both hypertension and bradycardia.

Why irregular breathing pattern?

The irregular breathing pattern seen in patients with elevated ICP is due to inadequate function of the respiratory control center located in the medulla oblongata, because of the reduced cerebral perfusion pressure, or direct damage to important structures. Often Cheyne-Stokes respirations are seen.

Sources:

https://umem.org/educational_pearls/133/

http://en.wikipedia.org/wiki/Cushing's_triad

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Welcome to Emergency Medicine 1

Welcome to Emergency Medicine 1, a blog about pre- and intrahospital emgency medicine and traumatology. This blog is written by a Norwegian medical student and Emergency Medical Technician. The blog is aimed at students, doctors, nurses, EMTs, paramedics and other health professionals provding care for the critically ill or ingjured patient outside of or inside the hospital.

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