Albumin for Resuscitation in Critical Illness


A 50-year-old man was brought to the emergency department. He had sustained a burn affecting 55% of his total body surface area and a significant inhalational injury.  In the emergency department he was intubated and ventilated, central venous, arterial and urinary catheters were placed and resuscitation begun using the Parkland formula.

He was transferred to burns intensive care.  Fluid resuscitation was continued using Hartmann’s solution.  A bronchoscopy was performed; 1.26% sodium bicarbonate was used for lavage.  He became increasingly tachycardic and hypotensive.  He was oliguric.  His haematocrit was 0.45.  Fluid status was difficult to assess clinically; he felt warm to touch.  An oesophageal Doppler probe was sited which demonstrated low stroke volume and corrected flow time.  His Doppler parameters improved with each 250ml bolus of Hartmann’s solution but the effect was short lived.  Noradrenaline and then adrenaline infusions were used in an attempt to maintain blood pressure.  After a significant volume of crystalloid had been given, approximately 12 hours after the time of injury, 4.5% human albumin solution was requested.  This seemed to have a more prolonged effect than Hartmann’s solution.  Over the next 12 hours the patient’s haemodynamic status stabilised and he was able to undergo initial surgical management of his burn 36 hours after presentation.

What is the evidence for the use of human albumin solution for fluid resuscitation in critically ill patients.Read More »

Management of Refractory Intracranial Hypertension

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?
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Steroids in Cervical Spine Injury

Steroids in Cervical Spine Injury

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 »

Tourniquets in Severe Traumatic Limb Haemorrhage

Tourniquets in Severe Traumatic Limb Haemorrhage

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?

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Lactate Physiology and Predicting Disease Severity

Lactate Physiology and Predicting Disease Severity

A middle aged man presented with urosepsis after several days antibiotic therapy in the community. He was in septic shock, with tachypnoea, tachycardia and hypotension. He had raised inflammatory markers and acute kidney injury. His initial lactate level was 14mmol/L with a significant metabolic acidosis (base deficit 21). He was commenced on iv antibiotics, noradrenaline and renal replacement therapy. Lactate levels cleared to less than 2mmol/L over the next 24hrs. He weaned off noradrenaline in 72 hours and CVVHDF over the next 5 days.

How is lactate produced and what is its significance in predicting the severity of critical illness?

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Tranexamic Acid in Trauma

Tranexamic Acid in Trauma

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?

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