Management Of TBI

Management Of TBI

Traumatic brain injury (TBI) is a major medical and socio-economic problem, and is the leading cause of death inchildren and young adults. The main objectives in managing TBI are prevention and treatment of intracranial hypertension and secondary brain insults, preservation of cerebral perfusion pressure (CPP), and optimization of cerebral oxygenation.

In general, TBI is divided into two discrete periods: 

• primary and 
• secondary brain injury
  

The primary brain injury is the physical damage to parenchyma (tissue, vessels) that occurs during traumatic event, resulting in shearing and compression of the surrounding brain tissue. 

The secondary brain injury is the result of a complex process, following and complicating the primary brain injury in the ensuing hours and days. Numerous secondary brain insults, both intracranial and extracranial or systemic, may complicate the primarily injured brain and result in secondary brain injury. Secondary, intracranial brain insults include cerebral edema, hematomas, hydrocephalus, intracranial hypertension, vasospasm, metabolic derangement, excitotoxicity, calcium ions toxicity, infection, and seizures. 

Secondary, systemic brain insults are mainly ischemic in nature , such as: 

• Hypotension (systolic blood pressure [SBP] < 90 mm Hg) 
• Hypoxemia (PaO2 < 60 mm Hg; O2 Saturation < 90%) 
• Hypocapnia (PaCO2 < 35 mm Hg) - Hypercapnia (PaCO2 > 45 mm Hg) 
• Hypertension (SBP > 160 mm Hg, or mean arterial pressure [MAP] > 110 mm Hg)
• Anemia (Hemoglobin [Hb] < 100 g/L, or hematocrit [Ht] < 0.30)
• Hyponatremia (serum sodium < 142 mEq/L)
• Hyperglycemia (blood sugar > 10 mmol/L)
• Hypoglycemia (blood sugar < 4.6 mmol/L)
• Hypo-osmolality (plasma osmolality [P Osm] < 290mOsm/Kg H2O)
• Acid-base disorders (acidemia: pH < 7.35; alkalemia: pH > 7.45)
• Fever (temperature > 36.5°C)
• Hypothermia (temperature < 35.5°C)

Critical care management of severe TBI

Objective : 

• Stabilization of the patient, if still unstable
• Prevention of intracranial hypertension
• Maintenance of an adequate and stable cerebral perfusion pressure (CPP)
• Avoidance of systemic, secondary brain insults (SBI)
• Optimization of cerebral hemodynamic and oxygenation

1. Analgesia, sedation and paralysis

Adequate sedation potentiates analgesics; provides anxiolysis; limits elevations of ICP related to agitation, discomfort, cough or pain; facilitates nursing care and mechanical ventilation; decrease O2 consumption, CMRO2, and CO2 production; improves patient comfort; and prevents harmful movements

2. Mechanical ventilation

The ventilatory settings should be adjusted to maintain a pulse oximetry (SpO2) of 95% or greater and/or PaO2 of 80 mm Hg or greater and to achieve normoventilation (eucapnia) with PaCO2 of 35 to 40 mm Hg , protective ventilation with low tidal volume and moderate positive end-expiratory pressure (PEEP) has been recommended to prevent ventilator-associated lung injury and increased ICP. 

Within the first 24 hoursfollowing severe TBI, hyperventilation should be avoided, as it can further compromise an already critically reduced cerebral perfusion. Excessive and prolonged hyperventilation results in cerebral vasoconstriction and ischemia. Thus, hyperventilation

is recommended only as a temporizing measure to reduce an elevated ICP. A brief period (15-30 minutes) of hyperventilation, to a PaCO2 30-35 mm Hg is recommended to treat acute neurological deterioration reflecting increased ICP. However, when hyperventilation is used, SjvO2 or PbtO2 measurements are recommended to monitor cerebral oxygenation and avoid cerebral ischemia.

Prior to suctioning the patient through the endotracheal tube (ETT), preoxygenation with a fraction of

inspired oxygen (FiO2) = 1.0, and administration of additional sedation are recommended to avoid desaturation and sudden increase in the ICP. Suctioning ETT must be brief and atraumatic.

3. Hemodynamic support

Hemodynamic instability is common in patients with severe TBI. Hypotension, defined as SBP < 90 mm Hg or MAP < 65 mm Hg, is a frequent and detrimental secondary systemic brain insult.

4. Anemia is a common secondary systemic brain insult and should be avoided, with a targeted hemoglobin ≥10.0 g/dL or hematocrit ≥0.30. Brain tissue is reach in thromboplastin and cerebral damage may cause coagulopathy. Coagulation abnormalities should be aggressively corrected with blood products as appropriate, especially in the presence of a traumatic intracranial hemorrhage.

5. Hypertension, defined as SBP > 160 mm Hg or MAP > 110 mm Hg, is also a secondary systemic brain insult that can aggravate vasogenic brain edema and intracranial hypertension. However, hypertension may be a physiological response to a reduced cerebral perfusion.

6. Cerebral perfusion pressure

Cerebral ischemia is considered the single most important

secondary event affecting outcome following severe TBI. CPP, defined as the MAP minus ICP, (CPP = MAP - ICP), below 50 mm Hg should be avoided. A low CPP may jeopardize regions of the brain with pre-existing ischemia, and enhancement of CPP may help to avoid cerebral ischemia. The CPP value to target should be maintained above the ischemic threshold at a minimum of 60 mm Hg.

7. Hyperosmolar therapy

Mannitol administration is an effective method to decrease raised ICP after severe TBI [80]. Mannitol creates a temporary osmotic gradient and it increases the serum osmolarity. The prophylactic administration of mannitol is not recommended. The effective dose

is 0.25-1 g/kg, administered intravenously over a period of 15 to 20 minutes. Hypertonic saline can be used as an alternative for manitol for the treatment of elevated ICP. 

8. Temperature Modulation 

Moderate systemic hypothermia at 32°C to 34°C, reduces cerebral metabolism and CBV, decreases ICP, and increases CPP. However , Evidence of the impact of moderate hypothermia on the outcome of patients with TBI was controversial. Fever should be aggressively treated in patients with severe TBI. 

9. Antiseizure prophylaxis 

Recommended prophylaxis therapy to prevent early post-traumatic seizure in TBI patients who are at high risk for seizures. The risk factors include : 

GCS score < 10, cortical contusion, depressed skull fracture, subdural hematoma, epidural hematoma, intracerebral hematoma, penetrating TBI, and seizures within 24 hours of injury. Phenytoin is the recommended drug for the prophylaxis of early post-traumatic seizures. A loading dose of

15 to 20 mg/kg administered intravenously (I.V.) over 30 minutes followed by 100 mg, I.V., every 8 hours, titrated to plasma level, for 7 days, is recommended.

10. Deep vein thrombosis prophylaxis

Severe TBI patients are at significantly high risk of developing venous thromoembolic events (VTEs) including deep vein thrombosis (DVT) and pulmonary embolism. Although, evidence to support recommendations regarding the timing of pharmacological

prophylaxis is lacking, most experts suggest initiating pharmacologic prophylaxis as early as 48 to 72 hours after the injury, in the absence of other contraindications.

11. Stress ulcer prophylaxis

Severe TBI is a well-known risk factor for stress ulcers

(Cushing’s ulcer) in the ICU. Prophylaxis includes early enteral feeding, and pharmacological prophylaxis such as H2- blockers, proton-pump inhibitors and sucralfate. 

12. Nutritional support

Severe TBI patients are usually in hypermetabolic, hypercatabolic and hyperglycemic state, with altered G.I. functions. The potential advantages of enteral feeding include stimulation of all gastro-intestinal tract functions, preservation of the immunological gut barrier function and intestinal mucosal integrity, and reduction of infections and septic complications.

13. Glycemic control

In patients with severe TBI, stress hyperglycemia is a common secondary systemic brain insult. Studies showed that hyperglycemia has repeatedly been associated with poor neurological outcome after TBI. Although hyperglycaemia is detrimental, maintaining low blood glucose levels within tight limits is controversial in patients with severe TBI, because hypoglycemia, a common complication of tight glucose control, can induce and aggravate underlying brain injury. 

14. Steroids

Steroids administration is not recommended for improving the outcome or reducing ICP in patients with severe TBI. Moreover, steroids may be harmful after TBI.

15. Fluids and electrolytes

The goal of fluid management is to establish and maintain euvolemia to moderate hypervolemia. Negative fluid balance has been shown to be associated with an adverse effect on outcome, independent of its relationship to ICP, MAP, or CPP. Isotonic crystalloids should be

used for fluid management, and normal saline (NS) is the recommended solution. Aggressive fluid resuscitation with NS may result in hyperchloremic metabolic acidosis, a predictable and important consequence of large-volume, saline-based intravenous fluid administration, with different clinical implication. 

General intensive care

Similar to other patients in the intensive care, TBI victims should receive the usual daily care as follows :

• Raising head of bed to 30° - 45°: that would reduce ICP and improves CPP [125]; and lower the risk of ventilator-associated pneumonia (VAP).
• Keeping the head and neck of the patient in a neutral position: this would improve cerebral venous
• drainage and reduce ICP.
• Avoiding compression of internal or external jugular veins with tight cervical collar or tight tape fixation of the endotracheal tube that would impede cerebral venous drainage and result in an increase in the ICP.
• Turning the patient regularly and frequently with careful observation of the ICP [126].
• Providing eye care, mouth and skin hygiene
• Implementing all evidence-based bundles for prevention of infection including VAP [127] and central line bundle 
• Administrating a bowel regimen to avoid constipation and increase of intra-abdominal pressure and ICP.
• Performing physiotherapy

Surgical Approach :

Surgical decompressive craniectomy has been suggested as a promising therapeutic approach for patients with acute severe TBI at risk to develop severe brain edema. Decompressive craniectomy and hemicraniectomy, both are well accepted for the surgical treatment of intractable intracranial hypertension in cases in which medical management fails.

Conclusion

The management of severe TBI centers on meticulous and comprehensive intensive care that includes multimodel, protocolized approach involving careful hemodynamic support, respiratory care, fluid management, and other aspects of therapy, aimed at preventing secondary brain insults, maintaining an adequate CPP, and optimizing cerebral oxygenation. This approach clearly requires the efforts of a multidisciplinary team including neurointensivists, neurosurgeons, bedside nurses and respiratory therapists, and other members of the medical team. While such management can be challenging, it is

by all means rewarding considering the age of the victims and the socio-economic impact of the problem.

Source : www.sjtrem.com