Traumatic Brain Injury Case Study - Discussion

Closed head injury

The cranium is a partially closed cavity that contains brain tissue, cerebral spinal fluid (CSF), cerebral blood volume (CBV), interstitial water, and intracellular water. The brain is able to maintain its own hemodynamic balance to some degree by shifting fluids from areas of high pressure to areas of low pressure. If intracranial pressure (ICP) goes up, the brain is able to shift CSF from the area of the cranium to the spinal canal and shift venous blood to the neck and chest veins. When a person has a head injury the most common side effect is swelling due to increased interstitial and intracellular waters.

To understand the management of closed head injury, the methods of monitoring must first be explained. There are two kinds of intracranial monitoring devices available. The first is the most invasive but gives the most accurate and immediate information. This is the intraventricular catheter. It enables the caregivers to have constant and continuous reliable readouts of the patient's intracranial pressure and also offers access to the CSF for removal to help maintain acceptable pressures. The second of the two is the subarachnoid monitor. It was devised to avoid the need to penetrate the brain tissue; however, this monitor offers much less reliable information and does not have the benefit of access to the CSF.

A patient with a closed head injury can present many airway management problems for the respiratory care practitioner, including (but not limited to) altered ventilatory drive and level of consciousness. There is a high risk of respiratory complications due to the location of the respiratory control center in the brain. Any swelling that may occur within the brain can impede transmission and/or function of this respiratory control mechanism. The three most common adverse effects are different respiratory patterns labeled Cheyne Stokes, Kussmaul, or apnea. Cheyne Stokes is a breathing pattern that has roller coaster trends of respiration that change in depth and rate. Kussmaul is a little different in that the breaths become very rapid and deep and stay that way. The last, and definitely the worst, is apnea. Apnea is a complete cessation of breathing.

The respiratory care practitioner may also be called upon to provide hyperventilation via mechanical ventilation. Hyperventilation causes pH to rise which in turn causes cerebral vasoconstriction. This allows less blood flow to the brain and reduces intracranial pressure. This therapy is achieved by increasing the patient's minute ventilation until the PaCO₂ reaches about 28 mm Hg, at which point a decrease in intracranial pressure is noted. However, this level of CO₂ can only be maintained for less than 24 hours, after which time the CO₂ level must be brought up to between 30 and 35 mm Hg. When providing this therapy it is critical that the patient's PaCO₂ should never drop below 20 mm Hg. At this level the cerebral perfusion pressure (CPP) is compromised by inadequate cerebral blood flow. To calculate CPP, subtract intracranial pressure from mean arterial pressure: CPP = MAP - ICP.

There have been shown to be four distinct benefits to limiting the period of hyperventilation: (1) avoiding the necessity for "stepwise" increases in CO2 when ventilator discontinuance is desired, (2) avoiding the loss in bicarbonate ions that results from long-term respiratory alkalosis, (3) providing an immediate decompression therapy if ICP suddenly rises during the illness, and (4) providing maximal cerebral blood flow. An important side note to this therapy is that keeping the patient elevated at 30 degrees maximizes cardiovascular function and reverses some of the adverse effects of PEEP. When the patient begins to improve, weaning from PEEP must be done very slowly and carefully. A gradual reduction in PEEP will reduce the risk of a sudden increase in venous return, cardiac output, arterial blood pressure, and cerebral blood flow.

The practice of hyperventilating patients with closed head injuries has changed, however. Recent studies have shown that hyperventilation may be less predictable in reducing cerebral blood flow than previously thought and may actually compromise perfusion.

The patient being examined in this case study exhibited extremely low levels of consciousness and impaired ventilatory drive. He presented the biggest challenge during weaning. Although the patient had adequate respiratory muscle strength, his tidal volume was low and his respiratory rate was high. There were significant episodes of apnea after extubation which required re-intubation.

Atelectasis

Atelectasis can be identified in a number of ways. During patient assessment the following findings are suggestive of atelectasis: increased tactile and vocal fremitus, dull percussion note, diminished breath sounds, crackles and whispered pectoriloquy. Common radiologic findings on a chest x-ray are: increased density in areas of atelectasis, air bronchograms, and elevation of the hemidiaphragm on the affected side. Dependent lung regions usually appear initially with areas of increased density. Large areas of atelectasis are more commonly associated with air bronchograms, elevation of hemidiaphragm, or mediastinal shift toward the affected side. Lung volumes are normally reduced due to atelectasis. The normal treatment for atelectasis is incentive spirometry to increase lung volume or inflate collapsed alveoli by increased mean airway pressure. During mechanical ventilation increased mean airway pressure can be accomplished by an increase in PEEP, peak inspiratory pressure, or inspiratory time. The underlying cause of atelectasis should be treated for full recovery. Although supplemental oxygen is prescribed, health care workers should be aware of the refractory hypoxemia due to capillary shunting. Supplemental oxygen should not, therefore, be the only therapy administered.