A 20 year-old man was admitted to his local district hospital with a severe head injury following an assault. On arrival in the Emergency Department he was agitated with a reduced conscious level, with evidence of blunt trauma to the head and neck. Prior to intubation, his Glasgow Coma Score (GCS) was recorded as 7 (E1V2M4), and with cervical spine precautions he underwent intubation with subsequent mechanical ventilation and sedation.
An urgent CT brain and cervical spine revealed early evidence of intracerebral contusions with diffuse areas of petechial intracerebral haemorrhage identified. Nasal and maxillary fractures were also seen, with no cervical spine pathology identified. He was transferred to the regional neurological centre for assessment and ongoing management.
On arrival in the Neurosurgical Intensive Care unit the patient underwent insertion of an intracranial pressure monitor revealing an intracranial pressure (ICP) of between 30-35 mmHg. Pupil reactivity was sluggish bilaterally. Sedation was changed to infusions of propofol, fentanyl and midazolam, positioning was optimised with 20 degree head-up tilt, endotracheal tube ties were replaced and targeted mechanical ventilation to EtCO2 4- 4.5kPa. Central venous access was established and an infusion of Noradrenaline was used to target cerebral perfusion pressure to 70mmHg.
Initial medical management stabilised ICP below 25mmHg, but within the next 12 hours this began to rise despite neuromuscular blockade and infusion of hypertonic saline. Further CT imaging revealed progression of the intracerebral contusions with developing oedema. The patient was transferred to the operating theatre for insertion of an external ventricular drain. CSF drainage resulted in an immediate but small improvement in ICP but again over the next 12 hours it began to rise, and decision was made for bifrontal decompressive craniectomy.
Subsequent recovery was slow and was complicated by ventilator-associated pneumonia, a protracted tracheostomy wean and severe agitation. The patient underwent intensive neuro-rehabilitation and had been decannulated, but was left with persistent cognitive impairment, seizures and depression.
What is the rationale for performing decompressive craniotomy in TBI?
A young man with no significant past medical history was admitted to the Emergency Department following an assault. His Glasgow Coma Score on arrival was 8 with a motor score of 4 and there was evidence of an external head injury. Pupils were symmetrically reactive. He was intubated to facilitate further management. Both primary and secondary surveys were unremarkable apart from multiple contusions to the face and scalp. Multi-slice CT showed no intrabdominal or intrathoracic injury but significant intracranial pathology with subarachnoid and intraventricular blood and multiple, principally frontal contusions. No associated neuraxial fracture was seen.
Urgent neurosurgical opinion was sought which confirmed no immediate target for surgical intervention. The patient was transferred to the intensive care unit where appropriate monitoring was established including the insertion of a fibreoptic subdural intracranial pressure bolt. Initial intracranial pressure was measured at 18 mmHg. Sedation with propofol and alfentanil infusions was titrated to a RASS score of -3, ventilation adjusted to a PaO2 > 13 kPa and PaCO2 4.5-5.0 kPa as per the Brain Trauma Foundation guidelines and an infusion of noradrenaline started to achieve a cerebral perfusion pressure of 60 mmHg. The patient was nursed 30° head-up and although active cooling was not undertaken, temperature maintained at less 35-37.5°C.
There was initial stability but approximately 24 hours after admission sustained rises in intracranial pressure (ICP) in excess of 25 mmHg were seen, necessitating boluses of sedation, the addition of atracurium by infusion, administration of hypertonic saline, cooling to 35°C and brief periods of hyperventilation to a PaCO2 4.0-4.5 kPa albeit without significant control. Urgent repeat CT brain was undertaken which showed evolution of the contusions with signifiant oedema and loss of both the lateral ventricles and basal cisterns.
On further consultation, neurosurgical colleagues again felt that no immediate surgical option was viable; in particular that attempts to insert and external ventricular drain were unlikely to be successful and that contusionectomy would produce significant disability. The patient was randomised into the RESCUEicp trial and thiopentone infusion started at a rate to produce isoelectrical activity on three lead electroencephalogram.
What are the management options for refractory intracranial hypertension? Read More »
A previously fit and well 46 year-old was admitted via the emergency department having sustained a neck injury whilst horse riding. She was unable to move her arms and legs immediately after the fall. On arrival to the Emergency Department, she was alert and orientated. Examination of the cardiovascular and respiratory system was unremarkable although there was evidence of diaphragmatic breathing.
Examination of her neurological system revealed:
•A sensory level at C6
•Absent upper limb reflexes except for brisk bicep reflex bilaterally
•⅖ power in shoulder abductors bilaterally
•Flaccid paralysis of her lower limbs
•No anal tone
She was initially managed in a hard neck collar with full spinal immobilisation. CT brain was reported to be normal. CT neck showed an obviously displaced fracture of C5 and C6 vertebral bodies. She was transferred to the intensive care unit for cardiovascular, respiratory and neurological monitoring while a definitive treatment plan was being considered. After discussions with the orthopaedic surgeons, it was decided not to commence high-dose steroids. This decision was reinforced after discussion with the local neurosurgical and spinal units. It was also decided not to surgically stabilise the c-spine due to the higher risk of respiratory complications. She was transferred to the spinal rehabilitation unit after 2 days.
What is the role of steroids in cervical spine injury?Read More »
A 30 year old male pedestrian was involved in a road traffic collision with a car travelling at speed. On arrival of the paramedics he was found to be unconscious with evidence of severe blood loss. He also had a partial amputation of his right leg below the knee. The paramedics applied a combat application tourniquet to the thigh, above the injury. He then suffered a cardiorespiratory arrest and CPR was commenced. On arrival in the emergency department his trachea was intubated and he underwent bilateral decompressive thoracostomies. Large bore intra-venous access was secured and two units of packed red cells given by a rapid infusion device. He remained haemodynamically unstable requiring a further six units of red cells and associated blood products to maintain a systolic blood pressure of above 80mmHg. Orthopaedic members of the trauma team were persistently keen to remove the tourniquet in order to prevent distal-neurovascular damage. This request was repeatedly denied and he was transferred rapidly to theatre for definitive control of his ongoing haemorrhage with an exploratory laparotomy. No cause for haemorrhage was found on laparotomy so attention shifted to damage control surgery on his leg in order to try and achieve some haemodynamic stability. Unfortunately to achieve this aim the tourniquet was removed. Bleeding was uncontrollable even with reapplication of the tourniquet and the patient exsanguinated and died.
What are the current recommendations for the use of limb tourniquets in trauma, and what is the evidence base for those recommendations?
A 40 year old male was brought into ED following a high speed road traffic accident. The patient was ejected from the vehicle. The patient was managed according to ATLS guidelines. He suffered extensive injuries including facial fractures, traumatic subarachnoid haemorrhage and multiple intra-cerebral haemorrhages, a flail chest and thoracic and cervical spine injuries. Once stabilised, the patient was transferred to the neurosurgical intensive care unit where an intra-cranial pressure (ICP) monitor was inserted to measure intracranial pressures. His ICP was persistently raised despite optimising respiratory parameters, deep sedation, muscle relaxation and then mannitol. A decision was made to commence an infusion of hypertonic saline 2.7% according to the local protocol. The ICP improved rapidly and stabilised and removed the need to proceed with surgical decompressive craniotomy.
What is the evidence for the use of hypertonic saline in the treatment of acutely raised intracranial pressure?Read More »
A 19 year old man experienced a head on collision as the driver of a car. He suffered significant lower limb open fractures, pelvic fractures, lung injuries and a small subarachnoid bleed. Initial management was performed in ED and included oxygen, IV access and fluid, lower limb and spine immobilisation, and analgesia. He underwent a trauma series CT scan, which identified the various injuries given above. At no point was his level of consciousness a concern, and he maintained his own patent airway throughout. He did not show signs of haemodynamic instability or evidence of life threatening haemorrhage. Tranexamic acid (TXA) was not given.
What is the evidence for using tranexamic acid in trauma?
A 35 year old man sustained a severe penetrating traumatic brain injury. His injuries were deemed to be unsurvivable, but he was not brainstem dead. He was on the organ donor register, and his family were keen to proceed with donation. He was admitted to the ICU to manage his end of life care and facilitate organ donation after circulatory death.
What are the eligibility criteria and contra-indications to organ donation after circulatory death?Read More »