Topic Progress:


The neurosurgeons intend to insert an extraventricular drain in Jake however there is a delay in theatres.   You stay in ED to help with Jake’s ongoing management.

What would be your resuscitation parameters when managing Jake while awaiting and EVD?

[az_accordion_section] [accordion title=”Answer” id=”acc-1″]

  • Maintain oxygen haemoglobin saturation (SaO2) 92-98%
  • Maintain SBP ≥ 110 mmHg (*note this is different to the Brain Trauma Foundation guidelines which state if aged 50-69 then > 100mmHg acceptable*)
    • Rationale for not adopting BTF blood pressure guidelines at RNSH:
  • Aim normocapnia (PaC02 35-40 mmHg) in the absence of transtentorial herniation or emergency management of elevated ICP
  • Continuous waveform capnography is required in all patients
  • 3% Saline or Mannitol solution can be used to treat intracranial hypertension or signs of transtentorial herniation[/accordion] [/az_accordion_section]


ICU Management 


  • Avoid or correct hypoxia immediately: maintain SaO2 92-98% 
  • Secure the airway with an ETT in patients who have moderate or severe TBI (GCS <12), in patients who are unable to maintain an adequate airway, and if hypoxia is not corrected by supplemental oxygen alone  


  • Monitor EtCO2 in intubated patients
  • Aim normocapnia (PaCO2 35-40mmHg)
  • Only use hyperventilation (to achieve PaCO2 < 35mmHg) if clinical signs of cerebral herniation, recognising that it is a temporising measure until definitive treatment (e.g. evacuation of haematoma) is achieved 
  • A PaCO2<35 mmHg is associated with cerebral vasoconstriction and a reduction in cerebral blood flow.
  • Cautiously apply Positive End Expiratory Pressure (PEEP) as high intrathoracic pressures may reduce cardiac output (and cerebral blood flow), and increase the central venous pressure and thus intracranial  pressure may rise:  generally aim PEEP < 10cmH2O

Blood Pressure

  • Fluid resuscitation with 0.9% sodium chloride to avoid hypotension, or to limit hypotension
  • Use vasopressors with caution
  • SBP should be either   100 mmHg if aged 50-69 or 110 mmHg for all other adult age groups (based on Brain Trauma Foundation Guidelines)
  • If concomitant penetrating trauma, blood pressure targets may need to be adjusted

Based on the SAFE trial subgroup analysis, 4% albumin may be harmful in TBI and crystalloid infusions (0.9% sodium chloride) should be administered as the first line resuscitation fluid.

Exclude hypoglycaemia

  • An altered mental state  may be due to hypoglycaemia
  • Target BGL of 6-10 mmol/L.


  • Mannitol 20% (0.25-1 g/kg) or  hypertonic saline (sodium chloride 3% (3 ml/kg)) is used if features of imminent cerebral herniation or in the management of refractory intracranial hypertension. 
  • There is no evidence to support the use of mannitol over hypertonic saline. 
  • Mannitol may contribute to hypotension through the osmotic diuresis that occurs
  • Hypertonic saline, though less haemodynamically volatile, may contribute to cellular injury (including central pontine demyelination) and renal failure.

 [az_accordion_section] [accordion title=”How does mannitol exert its effect?” id=”acc-1″]

Mannitol is thought to exert its effect by two means:

  • A rheological effect, mediated through an immediate plasma volume expanding effect that reduces haematocrit, reduces blood viscosity, increases CBF, and possibly increases cerebral oxygen delivery
  • An osmotic effect, owing to it being an osmotically active alcohol that will increase extracellular tonicity.
    • The osmotic effect of mannitol is delayed for 15-30 minutes and may persist for a variable period between 90 minutes and 6 hours. 
    • Hypovolemia should be avoided by adequate fluid replacement.[/accordion] [/az_accordion_section]

Sedation and Analgesia

There is a distinction between analgesia, sedation and anaesthetic agents. Analgesics and sedatives have limited ability to reduce ICP beyond suppressing pain, coughing and agitation. The anaesthetic induction agents e.g. thiopentone and propofol can produce specific physiological effects such as reducing ICP and cerebral oxygen demand

Sedation can help control intracranial pressure, but there have been no positive studies reporting on the influence of sedation on patient-centred outcomes from severe TBI.

Sedation benefits:

  • Improved patient comfort whilst ventilate
  • Helps control unnecessary movements (e.g. shivering) and suppresses coughing
  • Indirectly reduces oxygen demand
  • Acts as a sympatholytic
  • Suppresses seizure activity.
  • Indirect therapeutic effects of sedation include reducing cerebral oxygen demand and metabolism, preventing free radical formation and possibly improve coupling of regional blood flow to demand.

Sedation hazards:

  • Can hinder accurate assessment of neurology
  • May cause hypotension or myocardial depression
  • May prolong the duration of mechanical ventilation
  • May contribute to delirium

Commonly Used Sedatives and Analgesics in ICU

[az_accordion_section] [accordion title=”Fentanyl” id=”acc-1″]


0.1-2 mcg/kg/hr


  • It is highly selective for m (mu) opioid receptors.
  • The drug acts within 2-5 minutes, but is short acting as it is rapidly redistributed.
  • It is highly lipid soluble and has a more rapid onset than morphine, but prolonged infusions may result in a longer duration of action as the drug is well absorbed into the tissues.
  • Its metabolism is via the liver to inactive metabolites, so is less problematic in renal failure.
  • Note: fentanyl is incompatible with thiopentone.[/accordion] [accordion title=”Morphine” id=”acc-2″]


0.01 mg-0.05 mg/kg/hr


  • Similar in mechanism of action to fentanyl, morphine acts on opioid receptors but is less specific for m, which results in a few side effects, such as itching, nausea and vomiting.
  • It is less commonly used as an infusion in neurointensive care but may be used as patient-controlled analgesia (PCA).
  • Its onset is 3-5 minutes and has a variable duration of action, especially in renal failure.
  • It is metabolised in the liver to active metabolites, and morphine-6-glucuronide tends to accumulate in renal failure.[/accordion] [accordion title=”Propofol” id=”acc-3″]


0.1-4 mg/kg/hr, generally not to exceed 250 mg/hr in any patient


  • Propofol (2,6-di-isopropylphenol) is a short-acting IV anaesthetic agent, presented as a 1% white emulsion.
  • The mechanism of action of propofol is unclear but thought to act in a similar manner to benzodiazepines on the GABA receptor.
  • Propofol remains the mainstay of sedation in Intensive Care owing to its predictable pharmacokinetics and favourable sedation properties.
  • It is given for induction of anaesthesia and sedation in ICU, with typical onset within 30 seconds.  Its offset is relatively rapid.
  • Sedation may be maintained as needed with a continuous infusion, but the infusion rate should never exceed 4 mg/kg/hr owing to the risk of propofol infusion syndrome.
  •  Despite being metabolised in the liver and cleared by the kidney, renal and hepatic disease do not appear to greatly influence the effects of the drug. [/accordion] [accordion title=”Midazolam” id=”acc-4″]

Dose: 0.01-0.2 mg/kg/hr


  • Midazolam is a short acting benzodiazepine.
  • It binds to specific benzodiazepine receptors facilitating the inhibitory actions of GABA, resulting in hypnotic, anxiolytic, and anticonvulsant activity.
  • The elimination half-life increases significantly in critical illness and in the presence of renal impairment, which may lead to prolonged narcosis.  For this reason, midazolam is typically used as an adjunct to propofol or as a second line agent.
  • Because of its anticonvulsant activity and its benign effects on the circulation it remains a very useful drug in Intensive Care, but may contribute to an increase in ventilated days and has been associated with an increased incidence of delirium, particularly in the elderly.
  • Flumazenil is a benzodiazepine antagonist (reversal agent), however it should not be used in neurointensive care as it may cause seizures.[/accordion] [accordion title=”Dexmedetomidine” id=”acc-5″]

Dose: 0.2-1.0 mcg/kg/hr (loading is 1 mcg/kg over 10 minutes, but this is not typically given in ICU as it may cause hypotension and bradycardia)


  • Similar in action to clonidine, it has greater affinity for the a2-receptor on the neuronal post-synaptic membrane, providing anxiolysis and analgesia.
  • The sedation profile appears to be suited to patients who are agitated but still require regular assessment of their neurology.
  • Although the mechanism is not fully understood, it provides ‘cooperative sedation’ where patients remain interactive and calm, but the degree of narcosis is not as profound and patients continue to breathe and are easily rousable.  This makes it ideal for use in Intensive Care as it may facilitate weaning of ventilation as it may be continued after extubation.
  • Side effects that limit its use: hypotension and bradycardia is relatively common, nausea and vomiting, and its role in sedation specifically for TBI is unclear.[/accordion] [accordion title=”Thiopentone” id=”acc-6″]Thiopentone may be used in the acute setting for induction of anaesthesia and rapid sequence intubation in the haemodynamically stable patient, however its use for routine sedation for traumatic brain injury is not recommended.

Thiopentone is covered in detail within the elevated ICP module.[/accordion] [/az_accordion_section]


Neuromuscular Blockade (NMB)

NMB Benefits:

  • Prevents surges in ICP by preventing coughing (particularly on suctioning) and shivering
  • Facilitates temperature control (cooling)
  • Indirectly reduces metabolic demand indirectly
  • Enables mandatory ventilation and manipulation of PaO2 and PaCO2

NMB Hazards:

  • Masking post-traumatic seizure activity
  • An association with the development of critical illness polyneuropathy (CIPN), although this has been challenged by more recent trials.

Commonly Used Neuromuscular Blocking Agents in ICU

[az_accordion_section] [accordion title=”Suxamethonium” id=”acc-1″]

Dose: 1-2mg/kg (total body weight) for rapid sequence intubation (RSI)



  • Suxamethonium is a short acting depolarising neuromuscular blocking agent.
  • It mimics endogenous acetylcholine and produces depolarisation at the neuromuscular endplate (NME), which prevents further neuromuscular transmission.
  • Its onset is immediate after arrival at the NME and after the characteristic ‘fasciculations’ are seen, and its effect may last 3-5 minutes.
  • Owing to its side effect profile and concerns about its effects on ICP it should be used cautiously in ICU.
  • Suxamethonium is contraindicated in patients with recent burns after the first 24 hours or spinal cord trauma causing paraplegia from approximately day 10 to day 100 after the injury, raised potassium levels, severe muscle trauma or a history of malignant hyperpyrexia.
  • In patients with a genetic deficiency of plasma cholinesterase (which breaks down suxamethonium), its effects may be prolonged (‘sux apnoea’) and may cause protracted neuromuscular blockade.
  • Suxamethonium should not be used as a continuous infusion. [/accordion] [accordion title=”Rocuronium” id=”acc-2″]

Dose: 1-1.2 mg/kg (ideal body weight) for RSI, or 0.3-0.6 mg/kg/hr as an infusion



  • Rocuronium has largely superseded suxamethonium for rapid sequence intubation in Intensive Care.
  • At a dose of 1.2 mg/kg it produces similar intubation conditions within 30-40 seconds.
  • Its duration of action is similar to cisatracurium, but prolonged in the presence of renal impairment. For this reason, it should not be used in patients with kidney disease.
  • The effects of an RSI dose of rocuronium are reversed by 16 mg/kg suggamadex. [/accordion] [accordion title=”Cisatracurium” id=”acc-3″]

Dose: 0.1-0.2 mg/kg as a bolus or as an infusion of 1-2 mcg/kg/min cistracurium besilate


  • Cisatracurium is the more physiologically active enantiomer of atracurium.
  • As a bolus its speed of onset is approximately 60-90 seconds, thus it is not ideal for rapid sequence intubation.
  • Its duration of action is variable, but is intermediate in duration, approximately 20-30 minutes.
  • The benefit of cisatracurium is that is causes less histamine release compared to atracurium and its metabolism is also independent of hepatic or renal dysfunction, which makes it more suited to Intensive Care. [/accordion] [/az_accordion_section]


ICP Control

Detailed medical and surgical management of elevated ICP is detailed in the ICP learning module

ICU General Supportive Care

[az_accordion_section] [accordion title=”What other considerations are important in the day-to-day care of ICU patients with a TBI?” id=”acc-1″]

  • Nutrition via oral or enteral route as early as possible
    • Hypermetabolism and nitrogen wasting occurs in response to brain injury – as such patients are particularly vulnerable to weight loss and muscle atrophy


  • Bowel management
    • Due to immobility, reduced enteral fluid intake and sedative drugs used in ICU, patients are particularly prone to development of constipation, which contributes to discomfort and delirium


  • Transfusion of packed red blood cells is recommended for Hb <90 g/L in the first 7 days
    • Anaemia following severe TBI is associated with worse neurological outcomes. There is limited evidence to guide the optimal transfusion threshold in TBI.


  • Aim normothermia (36.5-38 degrees).   Sedation +/- neuromuscular blockade may be required for active cooling in severe TBI with elevated ICP


  • DVT Prophylaxis:  mechanical prophylaxis +/- chemical prophylaxis (if able) and weekly surveillance lower limb venous dopplers
    • Patients with TBI are at risk from DVT and PE owing to their often-prolonged period of sedation and immobility, in addition to having invasive venous catheters and a relative hypercoagulable state.
    • There is ongoing controversy about the optimal timing of when to start heparin in TBI patients, especially those with multicompartmental or intraparenchymal injury.
    • The presence of ICP monitoring is not a contraindication to heparin, but the dose should be withheld prior to exchange or planned removal


  • Seizure Prophylaxis: levetiracetam 500 mg BD  for all patients with moderate to severe TBI if there are focal cortical contusions or haemorrhage
    • Post-traumatic seizures (PTS) are classified as early (occurring within 7 days of injury), or late (occurring after 7 days following injury).
    • Risk factors for developing post-traumatic seizures include:
      Cortical contusionSeizures immediately post injurySubdural/epidural/intracerebral haematoma
      Linear or depressed skull fracturePenetrating head injuryAge < 65 years
      Initial GCS < 10Chronic alcoholism 

      Post-traumatic amnesia > 30 min


    •  The Brain Trauma Foundation recommends that patients with TBI who are high risk for seizures (as above) be prescribed 7 days of phenytoin, with those not exhibiting seizures during this time having their drug ceased.  More recently, there has been a trend to move away from phenytoin due to its side effect profile, favouring levetiracetam.


  • Propranolol, clonidine or dexmedetomidine can be used for management of sympathetic ‘storming’ in TBI[/accordion] [/az_accordion_section]


Surgical Management

The overall goal of all surgical treatment is to prevent secondary injury by helping to maintain blood flow and oxygen to the brain and minimize swelling and pressure.

The surgical management depends on the injury.  We will look at the common traumatic brain injuries requiring surgical intervention below with the guidelines stated being provided by the Brain Trauma Foundation.


[az_accordion_section] [accordion title=”Acute Extradural (Epidural) Haematomas” id=”acc-1″]


EDH > 30 cm3 regardless of the patient’s GCS.


Craniotomy and evacuation of haematoma[/accordion] [accordion title=”Acute Subdural Haematomas” id=”acc-2″]


  • SDH with a thickness > 10 mm or a midline shift greater than 5 mm on CT scan should be surgically evacuated, regardless of the patient’s GCS.
  • All patients with acute SDH with a GCS < 9 should undergo ICP monitoring.
  • A patient with a GCS < 9 and a SDH < 10-mm thick and a midline shift < 5mm should undergo surgical evacuation of the lesion if the GCS score decreased between the time of injury and hospital admission by 2 or more points on the GCS and/or the patient presents with asymmetric or fixed and dilated pupils and/or the ICP exceeds 20 mm Hg


Craniotomy with or without bone flap removal and duraplasty.[/accordion] [accordion title=”Traumatic Parenchymal Lesions” id=”acc-3″]


  • Patients with parenchymal mass lesions and signs of progressive neurological deterioration referable to the lesion, medically refractory intracranial hypertension, or signs of mass effect on CT scan should be treated operatively.
  • Patients with a GCS of 6 to 8 with frontal or temporal contusions >20 cm3 in volume with midline shift of at least 5 mm and/or cisternal compression on CT, and patients with any lesion > 50 cm3 in volume should be treated operatively.


Decompressive procedures, including subtemporal decompression, temporal lobectomy, and hemispheric decompressive craniectomy, are treatment options for patients with refractory intracranial hypertension and diffuse parenchymal injury with clinical and radiographic evidence for impending transtentorial herniation.[/accordion] [accordion title=”Posterior Fossa Mass Lesions” id=”acc-4″]


Patients with mass effect on CT scan or with neurological dysfunction or deterioration as a result of the lesion should undergo operative intervention. Mass effect on CT scan is defined as distortion, dislocation, or obliteration of the fourth ventricle; compression or loss of visualisation of the basal cisterns, or the presence of obstructive hydrocephalus.


Suboccipital craniectomy is the predominant method reported for evacuation of posterior fossa mass lesions, and is therefore recommended.[/accordion] [accordion title=”Depressed Skull Fractures” id=”acc-5″]


  • Patients with compound skull fractures depressed greater than the thickness of the cranium should undergo operative intervention to prevent infection.
  • Patients with compound depressed skull fractures may be treated nonoperatively if there is no clinical or radiographic evidence of dural penetration, significant intracranial hematoma, depression greater than 1 cm, frontal sinus involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination.
  • Nonoperative management of closed depressed skull fractures is a treatment option.


Elevation and debridement is recommended as the surgical method of choice.[/accordion] [/az_accordion_section]

© 2024 RNSHICU Site by Off the Page & Oli Flower

Log in with your credentials

Forgot your details?