Trauma
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Question 127 of 180
A 20 year old rugby player is brought to ED with a head injury after a scrum collapsed at a rugby match. His GCS on admission is 6/15. He is intubated and stabilised and transferred to ICU. A few hours later, the patient deteriorates with rising blood pressure and bradycardia. What is your immediate management step?
Answer:
Raising the head of bed by 30 degrees reduces ICP and improves CPP without compromising cardiac output in euvolemic patients with traumatic brain injury. (N.B. In patients who are hypovolaemic, this may be associated with a fall in blood pressure and an overall fall in cerebral perfusion pressure.)Head Injury: Management
Trauma
Last Updated: 13th September 2022
Medical management
The basic principle of traumatic brain injury (TBI) treatment is that, if injured neural tissue is given optimal conditions in which to recover, it can regain normal function. Medical therapies for brain injury include intravenous fluids, correction of anticoagulation, temporary hyperventilation, mannitol, hypertonic saline, barbiturates, and anticonvulsants.
- Anaesthetics, analgesics, and sedatives
- Anaesthetics, sedation, and analgesic agents should be used cautiously in patients who have suspected or confirmed brain injury. Overuse of these agents can cause a delay in recognising the progression of a serious brain injury, impair respiration, or result in unnecessary treatment (e.g. endotracheal intubation). Instead, use short-acting, easily reversible agents at the lowest dose needed to effect pain relief and mild sedation.
- Low doses of IV opioids may be given for analgesia and reversed with naloxone if needed.
- Short acting IV benzodiazepines, such as midazolam, may be used for sedation and reversed with flumazenil if needed.
- Intravenous fluids
- To resuscitate the patient and maintain normovolaemia, trauma team members should administer intravenous fluids, blood, and blood products as required.
- Hypovolaemia in patients with TBI is harmful. Clinicians must also take care not to overload the patient with fluids, and avoid using hypotonic fluids. Moreover, using glucose-containing fluids can cause hyperglycaemia, which can harm the injured brain.
- Ringer’s lactate solution or normal saline is thus recommended for resuscitation.
- Carefully monitor serum sodium levels in patients with head injuries. Hyponatraemia is associated with brain oedema and should be prevented.
- Correction of anticoagulation
- Use caution in assessing and managing patients with TBI who are receiving anticoagulation or antiplatelet therapy.
- After obtaining the international normalised ratio (INR), clinicians should promptly obtain a CT of these patients when indicated.
- Rapid normalisation of anticoagulation is generally required.
- Temporary hyperventilation
- In most patients, normocarbia is preferred.
- Hypercarbia (PCO2 > 6.0 kPa) will promote vasodilation and increase intracranial pressure, and should therefore be avoided.
- Hyperventilation acts by reducing PaCO2 and causing cerebral vasoconstriction. Aggressive and prolonged hyperventilation can result in cerebral ischaemia in the already injured brain by causing severe cerebral vasoconstriction and thus impaired cerebral perfusion. This risk is particularly high if the PaCO2 is allowed to fall below 4.0 kPa.
- Use hyperventilation only in moderation and for as limited a period as possible. In general, it is preferable to keep the PaCO2 at approximately 4.5 - 5.0 kPa, the lower end of the normal range (4.5 kPa to 6.0 kPa).
- Brief periods of hyperventilation (PaCO2 of 4.0 to 4.5 kPa) may be necessary to manage acute neurological deterioration while other treatments are initiated.
- Hyperventilation will lower ICP in a deteriorating patient with expanding intracranial haematoma until doctors can perform emergent craniotomy.
- Mannitol
- Mannitol is used to reduce elevated ICP.
- The most common preparation is a 20% solution (20 g of mannitol per 100 ml of solution).
- Do not give mannitol to patients with hypotension, because mannitol does not lower ICP in patients with hypovolaemia and is a potent osmotic diuretic. This effect can further exacerbate hypotension and cerebral ischaemia.
- Acute neurological deterioration— such as when a patient under observation develops a dilated pupil, has hemiparesis, or loses consciousness—is a strong indication for administering mannitol in a euvolaemic patient. In this case, give the patient a bolus of mannitol (1 g/kg) rapidly (over 5 minutes) and transport her or him immediately to the CT scanner—or directly to the operating room, if a causative surgical lesion is already identified. If surgical services are not available, transfer the patient for definitive care.
- Hypertonic saline
- Hypertonic saline is also used to reduce elevated ICP, in concentrations of 3% to 23.4%; this may be the preferable agent for patients with hypotension, because it does not act as a diuretic.
- However, there is no difference between mannitol and hypertonic saline in lowering ICP, and neither adequately lowers ICP in hypovolaemic patients.
- Barbiturates
- Barbiturates are effective in reducing ICP refractory to other measures, although they should not be used in the presence of hypotension or hypovolaemia.
- Furthermore, barbiturates often cause hypotension, so they are not indicated in the acute resuscitative phase.
- The long half-life of most barbiturates prolongs the time for determining brain death, which is a consideration in patients with devastating and likely non-survivable injury.
- Barbiturates are not recommended to induce burst suppression measured by EEG to prevent the development of intracranial hypertension.
- High dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment. Haemodynamic stability is essential before and during barbiturate therapy.
- Anticonvulsants
- Posttraumatic epilepsy occurs in approximately 5% of patients admitted to the hospital with closed head injuries and 15% of individuals with severe head injuries.
- The three main factors linked to a high incidence of late epilepsy are seizures occurring within the first week, an intracranial haematoma, and a depressed skull fracture.
- Acute seizures can be controlled with anticonvulsants, but early anticonvulsant use does not change long-term traumatic seizure outcome.
- Anticonvulsants can inhibit brain recovery, so they should be used only when absolutely necessary.
- Currently, phenytoin and fosphenytoin are generally used in the acute phase. For adults, the usual loading dose is 1 g of phenytoin intravenously given no faster than 50 mg/min. The usual maintenance dose is 100 mg/8 hours, with the dose titrated to achieve therapeutic serum levels.
- Diazepam or lorazepam is frequently used in addition to phenytoin until the seizure stops.
- Control of continuous seizures may require general anaesthesia.
- It is imperative to control acute seizures as soon as possible, because prolonged seizures (30 to 60 minutes) can cause secondary brain injury.
- Prophylactic use of phenytoin or valproate is not recommended for preventing late posttraumatic seizures (PTS).
- Phenytoin is recommended to decrease the incidence of early PTS (within 7 days of injury), when the overall benefit is felt to outweigh the complications associated with such treatment. However, early PTS has not been associated with worse outcomes.
Surgical management
Surgical management may be necessary for scalp wounds, depressed skull fractures, intracranial mass lesions, and penetrating brain injuries.
- Scalp wounds
- It is important to clean and inspect the wound thoroughly before suturing. The most common cause of infected scalp wounds is inadequate cleansing and debridement.
- Blood loss from scalp wounds may be extensive, especially in children and older adults. Control scalp haemorrhage by applying direct pressure and cauterising or ligating large vessels. Then apply appropriate sutures, clips, or staples.
- Carefully inspect the wound, using direct vision, for signs of a skull fracture or foreign material. CSF leakage indicates that there is an associated dural tear.
- Consult a neurosurgeon in all cases of open or depressed skull fractures.
- Not infrequently, a subgaleal collection of blood can feel like a skull fracture. In such cases, the presence of a fracture can be confirmed or excluded by plain x-ray examination of the region and/or a CT scan.
- Depressed skull fractures
- For patients with depressed skull fractures, a CT scan is valuable in identifying the degree of depression and, importantly, excluding the presence of an intracranial haematoma or contusion.
- Generally, depressed skull fractures require operative elevation when the degree of depression is greater than the thickness of the adjacent skull, or when they are open and grossly contaminated.
- Less severe depressed fractures can often be managed with closure of the overlying scalp laceration, if present.
- Intracranial mass lesions
- Intracranial mass lesions should be managed by a neurosurgeon. If a neurosurgeon is not available in the facility that initially receives a patient with an intracranial mass lesion, early transfer to a hospital with neurosurgical capabilities is essential.
- In exceptional circumstances, a rapidly expanding intracranial haematoma can be imminently life-threatening and may not allow time for transfer if neurosurgical care is a considerable distance away, such as in austere or remote areas. Emergency craniotomy in a rapidly deteriorating patient by a non-neurosurgeon should be considered only in extreme circumstances. Surgeons properly trained in the procedure should perform this surgery, but only after discussing the lesion with and obtaining the advice of a neurosurgeon. There are few indications for a craniotomy performed by a non-neurosurgeon. This procedure is justified only when definitive neurosurgical care is unavailable.
- Penetrating brain injuries
- CT scanning of the head is strongly recommended to evaluate patients with penetrating brain injury.
- Plain radiographs of the head can be helpful in assessing bullet trajectory and fragmentation, as well as the presence of large foreign bodies and intracranial air. However, when CT is available, plain radiographs are not essential.
- CT and/or conventional angiography are recommended with any penetrating brain injury and when a trajectory passes through or near the skull base or a major dural venous sinus.
- Substantial subarachnoid haemorrhage or delayed haematoma should also prompt consideration of vascular imaging.
- Patients with a penetrating injury involving the orbitofacial or pterional regions should undergo angiography to identify a traumatic intracranial aneurysm or arteriovenous (AV) fistula; when an injury of this kind is identified, surgical or endovascular management is recommended.
- Magnetic resonance imaging (MRI) can play a role in evaluating injuries from penetrating wooden and other non-magnetic objects.
- The presence on CT of large contusions, haematomas, and intraventricular haemorrhage is associated with increased mortality, especially when both hemispheres are involved.
- Prophylactic broad-spectrum antibiotics are appropriate for patients with penetrating brain injury, open skull fracture, and CSF leak.
- Early ICP monitoring is recommended when the clinician is unable to assess the neurological examination accurately, the need to evacuate a mass lesion is unclear, or imaging studies suggest elevated ICP.
- It is appropriate to treat small bullet entrance wounds to the head with local wound care and closure in patients whose scalp is not devitalised and who have no major intracranial pathology.
- Objects that penetrate the intracranial compartment or infratemporal fossa and remain partially exteriorised (e.g., arrows, knives, screwdrivers) must be left in place until possible vascular injury has been evaluated and definitive neurosurgical management established. Disturbing or removing penetrating objects prematurely can lead to fatal vascular injury or intracranial haemorrhage.
- Burr hole craniostomy/craniotomy, which involves placing a 10- to 15-mm drill hole in the skull, has been advocated as a method of emergently diagnosing accessible haematomas in patients with rapid neurologic deterioration who are located in austere or remote regions where neurosurgeons and imaging are not readily available. Unfortunately, even in very experienced hands, these drill holes are easily placed incorrectly, and they seldom result in draining enough of the haematoma to make a clinical difference.
- In patients who need an evacuation, bone flap craniotomy (versus a simple burr hole) is the definitive life-saving procedure to decompress the brain. Trauma team members should make every attempt to have a practitioner trained and experienced in doing the procedure perform it in a timely fashion.
Brain death
A diagnosis of brain death implies that there is no possibility for recovery of brain function. Most experts agree that the diagnosis of brain death requires meeting these criteria:
- Glasgow Coma Scale score = 3
- Nonreactive pupils
- Absent brainstem reflexes (e.g. oculocephalic, corneal, and doll’s eyes, and no gag reflex)
- No spontaneous ventilatory effort on formal apnoea testing
- Absence of confounding factors such as alcohol or drug intoxication or hypothermia
Ancillary studies that may be used to confirm the diagnosis of brain death include:
- Electroencephalography: No activity at high gain
- CBF studies: No CBF (e.g. isotope studies, Doppler studies, xenon CBF studies)
- Cerebral angiography
Certain reversible conditions, such as hypothermia or barbiturate coma, can mimic brain death; therefore, consider making this diagnosis only after all physiological parameters are normalised and central nervous system function is not potentially affected by medications. Because children are often able to recover from extremely severe brain injuries, carefully consider diagnosing brain death in these patients. If any doubt exists, especially in children, multiple serial exams spaced several hours apart are useful in confirming the initial clinical impression. Notify local organ procurement agencies about all patients with the diagnosis or impending diagnosis of brain death before discontinuing artificial life support measures.
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
