This is the first of a regular posting of hypothetical cases based on real cases submitted to the Resuscitology Team for analysis and debrief on the Resuscitology Course. Course participants are asked: “Please describe a resuscitation case that you have been involved in or witnessed that you feel (a) either had great learning points for other people on the course or (b) you feel didn’t go as well as it should and would appreciate the chance to analyse and discuss it.”
Case details are removed or altered to guarantee anonymity and confidentiality while preserving learning points. Cases are shared with the permission of the submitting clinician.
This case discussion was facilitated and summarised by Chris Nickson
Male in his 20s, Motorcycle accident. No pre-arrival notification. Arrived in very busy ED (2 arrests ongoing including a paediatric arrest). Traumatic brain injury and cardiac arrest at scene then ROSC.
Patient suffered devastating head injury and severe chest trauma. Profoundly hypoxic, with SpO2 persistently in the 70s despite being intubated on 100% oxygen with bilateral intercostal catheters.
The CT showed severe subarachnoid haemorrhage and fractured skull and tonsillar herniation (coning). The patient’s (English speaking) family was overseas. It was a highly emotive situation with 3 cardiac arrests in ED within an hour.
Clinical Priorities in the Resus Room
The overall goals in this scenario include:
- Management of the entire ED, ideally so that multiple critical patients can receive optimal treatment (the senior doctor in charge of the ED may be best being “hands off” and maintaining situational awareness of the whole department)
- Optimally resuscitate the patient pending determination of whether palliation is appropriate as soon as possible. Key clinical priorities here are to:
- Address hypoxia, in light of a severe traumatic brain injury
- Expedite imaging to clarify diagnosis and prognosis
- Support staff during and after an extremely difficult situation
Aggressive resuscitation of a patient who is suspected to have non-survivable injuries can cause individual cognitive dissonance and tension within the team. In general, it is important to “resuscitate before you prognosticate”. It may help to explicitly state and acknowledge this openly with the team, e.g. “Team, this is a difficult situation. The patient may have non-survivable injuries, we need to determine this as soon as possible. Until we know for sure, we will resuscitate him as best we can.”
Causes of hypoxia in major trauma
In an intubated patient always remember to check DOPES first:
- Displaced endotracheal tube
- Obstructed endotracheal tube
- Patient factors
- Equipment (e.g. remove from ventilator)
- Stacked breaths (i.e. dynamic hyperinflation); Stomach (need NGT in small children as gastric distention can cause respiratory embarrassment); Synchrony (between patient and ventilator)
Patient factors in this case can be:
- Exacerbation of underlying disease (eg asthma), or
Causes of hypoxia resulting from major trauma include:
- Obstruction, injury
- Contusion, laceration, haemorrhage, pneumatocoeles
- Aspiration, Foreign bodies
- Acute Respiratory Distress Syndrome (ARDS)
- Pneumothorax (tension, open, closed), hemothorax, chylothorax
- Pulmonary embolism, fat embolism, pulmonary vascular injury
- Traumatic shunt or exacerbation of existing shunt (e.g. ASD/PFO, which can cause platypnea-orthodeoxia syndrome)
- CNS injury, spinal injury, phrenic nerve injury
- Severe hypercapnia (“CO2 filled lungs”) (e.g. due to brain impact apnoea prior to assisted ventilation)
- metHb causing falsely low SpO2 and “anaemic hypoxia” (smoke)
In Traumatic Brain Injury (TBI), proposed mechanisms of hypoxia (apart from brain impact apnea) include:
- Acute neurogenic pulmonary edema
- Sympathetically induced pulmonary vasoconstriction leading to V/Q mismatch
- Pulmonary shunting with changes in intracranial hypertension, e.g. passive opening of pulmonary arterio-venous shunts
Brain impact apnoea is a potential cause of death immediately after TBI. Such patients may have a normal, or near normal, CT brain and if adequately supported can make a full recovery. Without intervention, apnoea may lead to death.
Management of refractory hypoxaemia in a TBI patient
Observational studies consistently show that hypoxaemia is associated with worse outcomes including increased mortality following severe TBI. Evidence of harm from hyperoxia is less consistent. Current BTF guidelines do not specify a target SpO2 for severe TBI.
A step-wise approach to post-intubation hypoxaemia is described in LITFL’s Critical Care Compendium. Lung recruitment manoeuvres are controversial, and have primarily been studied as part of an open lung approach to mechanical ventilation in ARDS. They are worth considering as a rescue technique for refractory hypoxaemia with lung infiltrates as they can sometimes elicit a physiological response, even in the absence of ARDS (e.g. lung collapse), though it is uncertain if they improve patient outcomes. There are numerous other ways to improve oxygenation in ARDS, some of which could be considered in non-ARDS patients.
Unless there is obstructive lung disease (e.g. asthma, COPD), a protective lung ventilation strategy is generally appropriate for both ARDS and non-ARDS patients (e.g. patients with pulmonary contusions). For example, low tidal volumes (4-8 mL/kg PBW with plateau pressures <30 cmH20). However, this approach typically allows for permissive hypercapnia, which is not optimal for TBI patients as hypercapnia promotes cerebral vasodilatation and raised intracranial pressure (ICP) (Della Torre et al, 2017). High PEEP settings can be used to treat hypoxia in TBI patients, despite a raised ICP. However, excessive PEEP sometimes worsens oxygenation (e.g. overdistention in unilateral disease may increase shunt). In lungs with normal compliance, usually no more than 25% of the PEEP is transmitted to the central veins. In poorly compliant lungs (e.g. ARDS) very little PEEP is transmitted to the ICP. A small study found that PEEP up to 15 cmH20 has minimal changes in ICP and no change in CPP with normal lungs (McGuire et al, 1997). Furthermore, another small study showed that PEEP up to 15 cmH20 improves brain tissue oxygenation in severe TBI patients with ARDS (Nemar et al, 2017). A greater concern is the effect of PEEP on haemodynamics (Doblar et al, 1981). High PEEP – especially in hypovolaemic patients (e.g. haemorrhage) and patients with right heart failure – can decrease venous return, decreasing cardiac output and MAP. The decrease in MAP will decrease CPP and contribute to secondary insults in TBI. However, the decrease in MAP from PEEP can usually be prevented or corrected by appropriate use of vasopressors (e.g. noradrenaline) and fluid resuscitation (e.g. blood in a trauma patient). Overall, a PEEP of 15 cmH20 appears safe in TBI patients, and higher levels of PEEP could be considered in patients with refractory hypoxaemia as the harm from hypoxaemia may outweigh the potential harm from raised ICP and correctable effects on MAP.
In TBI, maintain cerebral perfusion pressure (CPP = MAP – ICP) in usual ways and decrease O2 consumption:
Head at 30 degrees (or greater if severely increased ICP) Avoid neck constrictions (e.g. loosen C-spine collar and ETT ties if needed)
- Avoid hypoxia (e.g. target SpO2 >95%) with FiO2 and PEEP (up to 15cm H20, consider higher if needed)
- Target PCO2 35-40 mmHg (avoid both hyperventilation and hypoventilation)
- Assume ICP 20 mmHg, so need MAP 80-90 mmHg for CPP 60-70 mmHg
- Noradrenaline to maintain MAP (+/- ongoing haemostatic resuscitation if needed)
- Consider hypertonic saline or mannitol, if ICP >20 mmHg or evidence of coning
- Sedation and paralysis
- Maintain euthermia (T 36-37C)
- Blood glucose 6-10 mmol/L
Resuscitation room palliation
The CEASE mnemonic has been proposed as a systematic approach to discontinuing resuscitation:
- Clinical factors
- Effectiveness of resuscitation
- Ask others (but not family)
- Stop resuscitation efforts
- Explain to family
The decision to take the patient to the CT scan, even with suboptimal oxygen saturations, is appropriate.
- CT brain confirms the severity of the TBI and impending coning
- provides closure for team and family
- If patient comfort is maintained, the harm to the patient is minimised, and the risk of incorrect diagnosis/ prognosis is avoided (e.g. atropine given pre-hospital for bradycardia causing “fixed dilated pupils”)
Attempts to optimise oxygenation should be time-specified and task-specified. If all reasonable options have been tried, and sufficient time allowed to check for improvement, then it is important not to “flail” but to proceed to the next step (CT brain to confirm diagnosis and guide ongoing management).
The mantra “resuscitate before you prognosticate” applies. In this situation, there may be tension in the team between ongoing attempts at aggressive resuscitation and the expectation of probable palliation. Aggressive therapy should continue until the appropriateness of palliation is confirmed. Furthermore, if the patient’s wish was to be an organ donor, ongoing organ support will be in the patient’s interest even after brain death.
Prognosis is always challenging, and should involve a neurosurgical opinion. We should avoid giving up hope purely on the basis of “bilaterally fixed dilated pupils”, because favourable outcomes are possible (Scotter et al, 2015) (especially if an extradural haemorrhage is present).
Palliation can be performed in the emergency department, but suitability is context-dependent (e.g. clinical suitability, how busy the ED is, available quiet space and meeting rooms, family dynamics, etc). Transfer to ICU for ongoing care and/or consideration of organ donation may be appropriate.
Breaking Bad News on the Telephone
The first rule of breaking bad news is: do not do it over the phone. However, in some situations – such as family being overseas – it is unavoidable.
Here is an approach:
- Rehearse before making the call (e.g. with a social worker, or someone else skilled in difficult conversations)
- Although this needs to be done in a timely fashion, delay the phone call until you are psychologically prepared if at all possible
- Check the identity of the patient and the identity of the NOK, including contacts details
- Introduce yourself clearly (Name, Role, Hospital)
- Check that you are speaking to the right person and that he or she is an adult
- Be direct and compassionate, use the “D word” – for example say “I’m sorry that I have to tell you the worst possible news. Your son, Mike, died in a car crash tonight.”
- Check if they have support… if they don’t, offer to call someone for them
- Provide follow up (e.g. social worker contact number)
Hot tip (from Vera Sistenich):
- The person involved in an emotionally draining resuscitation doesn’t have to be the person who breaks bad news to the family.
- A senior colleague who was not emotionally involved in the case may be better placed to have the discussion.
Team Debrief and Counselling
After an arrest, make sure loose ends are TIED up:
- Team check (is everyone OK?)
- Ingest and imbibe (if possible, take a break to eat, drink, and recharge)
- Equipment resupply (be ready the next emergency)
- Debrief (soon after the event)
You might also want to conduct a “pause”. Taking a moment as a team to acknowledge the life of the person who has died and the efforts of the team in trying to save them.
“Team check” means checking in on how team members are coping. They may say they are fine, but look for signs of stress or distress. If present, affected team members may need to take a break or even go home early.
An approach to “hot debriefs” (immediately after the event), along with links to references on the topic, is described on INTENSIVE. “Closing the loop” after the “hot debrief” should include checking in on people affected by the event and providing access to counselling, following up a patient’s outcome, reporting a sentinel event, or instigating a guideline change.
Bartels J. About the Medical Pause. ThePause.me. Accessed 12 May 2018. Available at URL: https://thepause.me/2015/10/01/about-the-medical-pause/
Della Torre V, Badenes R, Corradi F, et al. Acute respiratory distress syndrome in traumatic brain injury: how do we manage it?. J Thorac Dis. 2017;9(12):5368-5381. Available at URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5756968/
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Mcguire G, Crossley D, Richards J, Wong D. Effects of varying levels of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure. Crit Care Med. 1997;25(6):1059-62. [pubmed]
Nemer SN, Caldeira JB, Santos RG, et al. Effects of positive end-expiratory pressure on brain tissue oxygen pressure of severe traumatic brain injury patients with acute respiratory distress syndrome: A pilot study. J Crit Care. 2015;30(6):1263-6. [pubmed]
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Nickson CP. Lung recruitment manoevres. Critical Care Compendium, Lifeinthefastlane.com. Accessed 12 May 2018. Available at URL: https://lifeinthefastlane.com/ccc/recruitment-manoeuvres-in-ards/
Nickson CP. Platypnea-Orthodeoxia Syndrome. Critical Care Compendium, Lifeinthefastlane.com. Accessed 12 May 2018. Available at URL: https://lifeinthefastlane.com/ccc/platypnea-orthodeoxia-syndrome/
Nickson CP. Post-intubation hypoxia. Critical Care Compendium, Lifeinthefastlane.com. Accessed 12 May 2018. Available at URL: https://lifeinthefastlane.com/ccc/post-intubation-hypoxia/
Nickson CP. Improving Oxygenation in ARDS. Critical Care Compendium, Lifeinthefastlane.com. Accessed 12 May 2018. Available at URL: https://lifeinthefastlane.com/ccc/improving-oxygenation-in-ards/
Nickson CP. Breaking Bad News to Relatives. Critical Care Compendium, Lifeinthefastlane.com. Accessed 12 May 2018. Available at URL: https://lifeinthefastlane.com/ccc/breaking-bad-news-relatives/
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