A FFICM station on MedMock, start to finish

Good morning. We'll begin with the first question. A 34-year-old man has been admitted to your neurosciences critical care unit at a major trauma centre after a motorcycle collision. His GCS at the scene was 6 and the pre-hospital team intubated him. His CT head shows diffuse swelling with several small contusions but no lesion needing surgery, and his other injuries are minor. What are your priorities in the first few hours of his care?

My overriding aim is to prevent secondary brain injury. I'd start with a structured handover and reassessment: tube position and ventilation, pupils, the trauma CT report, and I'd keep spinal precautions until his spine is formally cleared. Then I'd set explicit neuroprotective targets. A PaO2 above 13 kPa, and a PaCO2 of 4.5 to 5.0 kPa, checked on arterial gases rather than relying on end-tidal CO2. Avoiding hypotension is critical, so an arterial line, and noradrenaline if needed, aiming for a systolic of at least 110 mmHg, which is the Brain Trauma Foundation threshold for his age, until an ICP monitor lets me target cerebral perfusion pressure. Head up about 30 degrees, neck neutral, and the tube ties and any collar checked so they don't impede venous drainage. Adequate sedation and analgesia, typically propofol and an opioid, so he isn't coughing or fighting the ventilator. Normothermia, actively treating any fever. Sodium kept in the normal range, avoiding hypotonic fluids, and glucose kept roughly between 6 and 10 mmol per litre. I'd watch for seizures, with a low threshold for EEG, start mechanical thromboprophylaxis, and plan ICP monitoring with the neurosurgeons.

You mentioned ICP monitoring. Is it indicated here, and which device would you choose?

Yes. He has a severe traumatic brain injury with an abnormal CT, which is the classic indication. He's sedated, so we've lost the clinical examination, and the Brain Trauma Foundation guidance supports managing severe injury using information from ICP monitoring. There are two main options. An external ventricular drain is the reference standard: it measures global pressure, can be re-zeroed, and lets you drain CSF as a treatment. But it carries a higher risk of infection and of haemorrhage along the tract, and with diffuse swelling the ventricles are often small, which makes it harder to place. An intraparenchymal monitor, placed through a bolt, is quicker and has a lower infection risk, but it's zeroed only once, at insertion, so it can drift; it measures local rather than global pressure; and it can't drain CSF. With diffuse swelling I'd favour a parenchymal monitor, but that's a joint decision with the neurosurgeon. Once it's in, I'd aim for a CPP of 60 to 70 mmHg and treat a sustained ICP above about 22 mmHg, the Brain Trauma Foundation threshold, although many UK units use 20.

The monitor is in. Over the next hour his ICP rises to a sustained 28 mmHg, with a CPP of 58 mmHg. How would you manage this?

First I'd go to the bedside and make sure it's real: look at the waveform and the trend, check his pupils, and look for simple causes, such as coughing or ventilator dyssynchrony, inadequate sedation, tight ties, his head position, a rising PaCO2 or falling oxygenation, fever, a low sodium, or seizures. I'd arrange an urgent repeat CT, because a new or expanding haematoma needs surgery, not escalating medical treatment. Alongside that I'd follow a tiered approach, as in the SIBICC consensus. Tier one: deepen sedation and analgesia, bring the PaCO2 to the lower end of normal, restore the CPP to at least 60 with noradrenaline, and give a bolus of hyperosmolar therapy, either hypertonic saline or mannitol, checking sodium and osmolality. If there were an EVD I'd drain CSF, and I'd get an EEG to exclude non-convulsive seizures. If the ICP stays high, tier two includes neuromuscular blockade, a short period of mild hypocapnia, and a supervised MAP challenge to see whether raising his blood pressure brings the ICP down, which tells me about his autoregulation. Tier three is a barbiturate coma with EEG monitoring, secondary decompressive craniectomy, or mild hypothermia, and I'd decide on those with my consultant and the neurosurgeon. Throughout, I'd avoid steroids, which increased mortality in the CRASH trial, and prolonged deep hyperventilation, which risks cerebral ischaemia.

Despite tier two measures, his ICP remains above 25 mmHg. The neurosurgeon raises decompressive craniectomy. What does the evidence say about craniectomy, and about therapeutic hypothermia, in this setting?

There are two key craniectomy trials. DECRA studied early bifrontotemporoparietal craniectomy in diffuse injury when the ICP had been above 20 mmHg for more than 15 minutes within an hour, despite first-tier treatment. It lowered ICP and shortened ICU stay, but functional outcome at six months was worse, so early craniectomy for moderate intracranial hypertension isn't supported. RESCUEicp is closer to this man: craniectomy as a last-tier treatment for ICP above 25 mmHg despite other measures. It substantially reduced mortality, but more of the survivors were in a vegetative state or severely disabled and dependent on others. So it's a values-based decision. It's a reasonable option for him, but he lacks capacity, so it's a best-interests decision, and before proceeding I'd want his family to hear from the neurosurgeon and me that it may save his life at the cost of severe disability, and I'd explore what he would have wanted. On hypothermia, Eurotherm3235 cooled patients to 32 to 35 degrees to control raised ICP and found worse functional outcomes, and POLAR found that early prophylactic hypothermia didn't improve outcome either. So I'd keep him strictly normothermic, and consider mild hypothermia only as a last-tier measure.

Thank you. Let's move on to the second question. A 52-year-old woman is on day two of an admission with acute gallstone pancreatitis. The surgical team refer her to you because she's increasingly breathless on escalating oxygen, her creatinine has risen sharply, and she remains hypotensive despite fluid. How would you assess the severity of her pancreatitis?

I'd use the revised Atlanta classification, which defines severity by organ failure and complications. Organ failure is assessed with the modified Marshall score, looking at respiratory, renal and cardiovascular function, and she appears to have failure in all three already. If it persists beyond 48 hours, she has severe acute pancreatitis, which carries the highest mortality; if it resolves within 48 hours, it's moderately severe. Predictive tools, such as the Glasgow-Imrie score, APACHE II, or a CRP above 150 at 48 hours, are most useful earlier on, to flag who's likely to deteriorate, but she's already declared herself. I'd also look for local complications. An ultrasound confirms gallstones and shows whether the bile duct is dilated. A contrast-enhanced CT is best done at least 72 to 96 hours after symptom onset to assess necrosis and collections, unless the diagnosis is uncertain or I'm worried about a complication such as bleeding or bowel ischaemia, when I'd scan sooner.

She's admitted to your unit and later needs intubation. Talk me through the key elements of her management over the next few days.

It's largely supportive, so I'd go system by system, with early advice from the specialist pancreatic centre in our network, as NICE advises for systemic complications. Respiratory: lung-protective ventilation, as ARDS is common here. Circulation: I'd resuscitate with a balanced crystalloid, but goal-directed, not aggressive. The WATERFALL trial found that aggressive fluid resuscitation caused more fluid overload without improving outcomes, and in pancreatitis excess fluid also worsens gut oedema and intra-abdominal pressure. So I'd give fluid against clear endpoints, using cardiac output monitoring, lactate and urine output, and support her blood pressure with noradrenaline rather than keep giving fluid. Renal: avoid nephrotoxins, and renal replacement therapy for the usual indications. Analgesia: this is very painful, so good opioid-based analgesia, which is part of her sedation while she's ventilated. Nutrition: early enteral feeding, started within 72 hours as NICE recommends for severe disease. Nasogastric feeding is usually tolerated, nasojejunal if it isn't, and parenteral nutrition only if enteral feeding fails or is contraindicated. Antibiotics: no prophylactic antibiotics, which NICE advises against, but a low threshold to look for and treat infection, including infected necrosis later on. And the basics: thromboprophylaxis, glucose control, and regular intra-abdominal pressure measurement, because she's at high risk of compartment syndrome.

On day five she's ventilated with rising airway pressures, she's become oliguric, and her abdomen is tense and distended. Her bladder pressure is 24 mmHg. What's happening, and how would you manage it?

This looks like abdominal compartment syndrome, which is a sustained intra-abdominal pressure above 20 mmHg with new organ dysfunction, here respiratory and renal. First I'd confirm the reading: measured with her supine, at end-expiration, zeroed at the mid-axillary line, with no active abdominal muscle contraction, and repeated rather than acting on a single value. Then I'd work through the medical measures in the WSACS guidance. Improve abdominal wall compliance with deeper sedation and analgesia, and a trial of neuromuscular blockade. Decompress the gut with a nasogastric tube on free drainage and a rectal tube, and pause enteral feeding for now. Look for drainable fluid with ultrasound or CT, because percutaneous drainage of ascites or a collection can bring the pressure down. And stop the positive fluid balance, removing fluid with diuretics or on renal replacement therapy once she's haemodynamically stable. I'd also recognise that the high airway pressures partly reflect a stiff abdomen and chest wall, not just her lungs. I'd involve the HPB surgeons early, because if the pressure stays above 20 with worsening organ failure despite these measures, she needs a decompressive laparotomy with a temporary abdominal closure.

Thank you. That's the end of the station.