Your aeromedical EMS crew is dispatched to Mexico for a head injury patient who's an American citizen being repatriated back home.
The patient is a 47-year-old male who was found unresponsive on the side of the road in Mexico the previous day and was diagnosed with a subarachnoid hemorrhage. It's unclear what happened, but the patient may have fallen or been hit by a car. There are no signs of external trauma noted. He was brought to the local clinic where surgery was performed for a subarachnoid hemorrhage.
On arrival, the crew finds an intubated male with a Glasgow coma scale (GCS) of 3 with pupils of 4 mm and nonreactive bilaterally. On physical exam, the crew notes a Foley catheter coming from his skull with a glove containing serosanguinous fluid tied to the other end. The Foley catheter was placed within the patient's ventricle in an attempt to drain cerebral spinal fluid (CSF) and decrease intracranial pressure.
The patient has no intracranial pressure monitoring (ICP) in place. His vital signs are as follows: Heart rate of 58, blood pressure of 135/67, respiratory rate of 16 on a ventilator, blood oxygen saturation (SpO2) of 100% with a fraction of inspired oxygen (FiO2) of 90%. A midazolam infusion is running for sedation.
Transportation from the clinic to the airport was initially arranged by means of a flatbed pick-up truck followed by a three-hour jet flight back to the United States.
The crew has concerns about cerebral herniation and doesn't want to drain more fluid off via the Foley catheter without knowing the ICP, understanding that draining too much fluid could be detrimental.
The decision is made to reduce ICP using a medication approach. Both hypertonic saline and mannitol are used clinically to reduce ICP; however, the clinic and the flight crew don't have access to either of the medications. After consultation with medical direction, the decision is made to use sodium bicarbonate mixed with normal saline to obtain 3% hypertonic saline solution. The patient is given the hypertonic saline solution with no increase of ICP and is able to complete the flight.
Increased ICP is a common problem faced by EMS providers when working with trauma patients with head injuries. An increase in ICP compresses the brain within the rigid skull, thereby reducing blood flow and worsening damage.
As the pressure in the head increases, the brain can no longer stay within the rigid skull and begins to herniate. On physical examination, this most often presents as posturing (decerebrate or decorticate) with increasingly nonreactive pupils and changes in vital signs such as bradycardia, hypertension and irregular respirations.
The Monro-Kellie doctrine states that the volume of contents within the skull: Brain, blood and CSF are constant. To maintain balance, an increase in one should cause a decrease in the other.1 After a traumatic insult to the brain, swelling of brain tissues ensues.
If the pressure is allowed to increase without change, the brain can herniate through one of the dural folds or, even worse, through the foramen magnum at the base of the skull. At the same time, it's important to optimize the patient's intravascular volume as well as mean arterial pressure to maintain adequate cerebral blood flow.
It's also important to prevent hypoxia, maintain eucapnia, and decompress the stomach as increases in intra-abdominal pressure can translate to other compartments.1 In the prehospital setting, it's difficult to optimize cerebral perfusion without intracranial pressure monitoring or medication to reduce cerebral swelling.
If the ICP remains high, cerebral injuries can worsen leading to poor neurological outcomes. Medications such as mannitol and hypertonic saline may be useful in reducing ICP. These medications work by increasing the osmolality of the blood thus pulling fluid from within the brain tissue to the intravascular space.
The theory is that the fluid involved in the brain swelling is exchanged for perfusion of oxygen-carrying blood to the damaged parts of the brain.
There are two different approaches for using medications to reduce swelling in the brain. Mannitol is a sugar that's not utilized or absorbed by the body and works by causing osmotic diuresis. The mechanism is similar to the way a patient with hyperglycemia has polyuria from the excess sugar within the blood stream.2
On the other hand, hypertonic saline pulls fluid from swollen tissue without causing the diuresis that can lead to hypotension and a decrease in cerebral perfusion pressure. Water passively follows the movement of sodium, thereby reducing the volume of fluid and swelling within the tissue.
Primary brain injury isn't possible for us to change, as this can only be altered through injury prevention. As EMS providers, we can prevent secondary brain injury by keeping our patients euoxic and eucapneic and optimizing cerebral perfusion pressure by maintaining an adequate BP and reducing ICP.
In the past, hyperventilation in deteriorating patients was thought to reduce ICP when no other means were unavailable. Current advance trauma life support (ATLS) guidelines recommend using this method in moderation for as limited a period as possible and only when the patient is showing lateralizing signs of herniation.1
Both mannitol and hypertonic saline aren't often available to EMS. Some critical care agencies carry these medications; however, they're often not the first to respond. Mannitol, as discussed, is a sugar that the body does not absorb; its clinical use is limited to lowering ICP. When the solution gets cool, it crystalizes and needs to be rewarmed prior to administration, which makes it difficult to use in the field.
Osmotic diuresis can also cause another problem: intravascular depletion and ultimately hypotension, which can worsen secondary brain injury.
Patients with head injuries can also develop diabetes insipidus (DI), which can complicate matters. This condition is caused by a loss of hypothalamic input of vasopressin and antidiuretic hormone, which causes the kidneys to retain fluid when in circulation. If the hypothalamus and pituitary gland are injured, this mechanism is lost and the patient can lose large volumes of fluid via urination. It can be difficult to clinically distinguish DI from the osmotic diuresis caused by mannitol, and mannitol can exacerbate this effect.
Hypertonic saline has multiple clinical uses. It can be used to correct hyponatremia and can be given as fluid in the setting of intravascular depletion. It requires a lower total volume of fluid administration than normal saline. It can be used to treat tricyclic antidepressant (TCA) overdoses.
Sodium bicarbonate is simply a different form of hypertonic saline and is carried by many EMS agencies. It's used to treat hyperkalemia, TCA overdoses and other conditions. Approximately 3% hypertonic saline can be obtained by mixing 300 cc of normal saline from a 500 cc bag with 200 mEq of sodium bicarbonate which translates to 4 ampules.
Two very promising studies show that when adults with head injury and increased ICP are given 85 mEq of 8.4% sodium bicarbonate over 20 minutes, they have results superior to 3% hypertonic saline for up to six hours. Another benefit of this treatment is that hyperchloremic acidosis isn't caused by the sodium bicarbonate solution, which is common with 3% hypertonic saline administration.3,4
Patients with traumatic head injuries are associated with high morbidity and mortality and are encountered by all EMS providers on a relatively regular basis. Some still practice permissive hypocapnia, which is often difficult to do and comes at other costs.
Sodium bicarbonate is a medication with many uses. It offers an accessible treatment choice to patients with signs of increasing ICP and is carried almost universally by EMS providers. It's cheap, easy to administer, a familiar medication and offers a simple way for EMS providers to decrease ICP.