FJFICM October 2007

FJFICM October 2007

This year, for the first time ever, the FJFICM was held in Perth. For what it's worth, here's what it was like for me.

Day 1 – the OSCE

With some 60 candidates, this was split up into two sittings, each of which was duplicated (i.e. 2 x 2 sittings of 15 candidates each), so the morning crew was quarantined until the afternoon crew had started their sitting. There were ten ‘active stations’ (six data interpretation, two cold cases, one communication station, and one ‘skill station’ that was actually more like a viva), and five rest stations spaced out so-as to bracket the four interactive stations. The stations were:

Haematology: four sets of data covering a DIC-like coagulation profile, a blood-film report that looked like a leukaemoid reaction, causes of macrocytosis with anisocytosis, and an intra-op ‘bleeder’ with results suggesting Von Willebrand’s.
Equipment: a pressure transducer with some ancillary questions, and two different types of trache tube (fenestrated, and flanged) – what would we use each of them for?
Microbiology: Causes of a bacterial-looking CSF, and treatment if it grew gram-positive bacilli; plus likely organisms and treatment for a multi-resistant gram-negative rod.
Respiratory function tests: lots of spirometry, pressure-volume loops, ventilator traces, what was wrong and what were we going to do about it?
Lots of X-rays – fairly straightforward (including causes of cavitating lung lesions), but more abnormalities than I could write down in ten minutes!
Lots of CT scans – ditto as for X-rays.
Communication station. I was somewhat frustrated with this station, as I usually enjoy them and like to think communication is one of my strong points. We were given a scenario of an elderly Maori gentleman with multiple comorbidities, admitted with respiratory failure and (apparently against his will) intubated and ventilated. We were to speak with a niece who had just flown in from NZ. The (very non-Maori) actress did a superb job of playing an aggressive relative who insisted it was Maori cultural belief that everything possible be done to keep him alive, including CPR in the most hopeless of circumstances. My frustration arose partly from the fact this simply doesn’t agree with my experience of Maori belief (in six months of Starship PICU), and partly from the fact that, in allowing her to lead the discussion, my ten minutes were up before I had the chance to make what I thought were some important points. But the examiners all smiled nicely, so hopefully they thought I’d done OK……….?
The ‘skill station’ was more like a viva, and consisted of a scenario of a gentleman in post-op cardiogenic shock with an intra-aortic balloon pump. We were then shown an IABP balloon, and quizzed on its structure; an IABP X-ray, and quizzed on landmarks; and some IABP tracings, and quizzed on timing. Also, what would we do if we saw blood coming up the drive line? And what were the pros and cons of inserting it with or without a sheath? Contra-indications and complications? What about anti-coagulation?
Cold case 1: this was a youngish lady with flagrant clubbing and cyanosis, a clear chest, no scars, a hyperdynamic apex, and surprisingly normal cardiac auscultation (perhaps a loud S1, definitely no murmur). In the absence of respiratory distress, I plumped for uncorrected congenital cardiac disease; then put my foot in it by saying possibly Eisenmenger’s (despite loud S1, not loud S2). The examiner gently steered me back on track by taking me through the differential of congenital cyanotic heart disease; but although I included the right diagnosis in my differential, it wasn’t until I bumped into the patient on the street afterwards that I learned she had TGA. I’m not sure whether I was really supposed to figure that out……….
Cold case 2: a lovely middle-aged gent who had supposedly presented with a PR bleed – “please examine his abdomen”. Smooth hepatomegaly, no spleen, no renomegaly, no ascites, no caput medusae, no jaundice, no flap, no spiders, no gynaecomastia, no testicular atrophy (yes, they made me examine them!), no haemorrhoids (they told me that for free), no clue. Had the chance once again to wade through a differential diagnosis, but never did learn the ‘real’ diagnosis.

Overall, I thought the OSCE was quite fair; interestingly, no biochemistry, ABGs or ECGS this sitting. I was very well-prepared for the data interpretation, and think I did pretty well there; I felt I let myself down on the cold cases through sheer lack of real-life preparation, and in the communication station just through bad luck; but nowhere had I crashed and burned, and things looked hopeful. From 2008 the OSCE will be dismantled: the data interpretation will be incorporated into the written papers, the communication and skill stations will move into the vivas, and the cold cases will be dropped entirely.

Day 2: Hot Cases

This got off to a bad start when I arrived at the Royal Perth Hospital, to discover that I had been given the wrong timetable and was supposed to be at Charles Gairdner on the other side of town. But the examiners were very apologetic, hustled me into a taxi, and got me there in plenty of time with no harm done. The two cases I got were pretty straightforward ‘ICU meat-and-drink’.

First up was a gentleman in his sixties who had fallen over, hit his head and sustained a base-of-skull fracture. He was now five days down the line – could I please comment on his likely prognosis? A craniectomy wound was obvious; although his ICP was fairly normal, he was still deeply sedated (no cough reflex), hypertonic with gross clonus, and on a substantial combination of anti-convulsants. The examiners’ questions were fairly straightforward; they showed me his CT (big craniectomy, residual subdural, lots of dead brain), and also an AXR (purportedly his) with a Seldinger wire lost up the IVC – what would I tell his wife about this? I opted to tell her everything – they seemed happy with this, but asked was there ever a circumstance when I wouldn’t inform about a medical mishap? The bell went while I was trying to decide on a suitable reply……..

Next was another elderly gentleman who had ‘gone septic’ after an elective open cholecystectomy and required intubation a week ago; he had failed weaning by becoming tachycardic, tachypnoeic and sweaty every time he lightened up, and had received a trache yesterday. I was asked to determine why he might be failing to wean. He responded appropriately to commands, and was only mildly weak; he had a dull and silent right base, good BP and urine output, and a systolic murmur that I couldn’t quite place but seemed to suggest HOCM (ejection murmur, loudest at LSB, didn’t radiate to carotids). I told the examiners I thought his weaning failure was multi-factorial: partly cardiac, partly due to a probable effusion at his right base, partly weakness due to critical care neuropathy, and maybe an element of septic encephalopathy which was now improving. They showed me his CXR, which showed no effusion but a high right hemi-diaphragm (presumably he had a sub-phrenic collection post cholecystectomy), then told me his renal chemistry was mildly deranged and asked for my opinion on his CT abdomen, which showed scarred and shrunken kidneys. A pair of ECGs showed rate-dependent ST-segment depression – how would I investigate this? And a quick tour through his blood gas, which showed a metabolic acidosis – mixed hyperchloraemic and anion-gap (though you had to correct the anion gap for the low albumin) – what did I think the missing anions were, given a normal lactate?

I thought the hot cases were surprisingly straightforward (after some of the exotic fare I’d practised on in Sydney!), and left feeling that as long as I didn’t completely stuff up the vivas, I should be in with a good chance.

Day 3: The Vivas

The vivas were held at a VERY posh-looking hotel (just next to the Australian Inventor of the Year awards – I never did find out what he/she had invented!). Again two sittings, each triplicated; with six viva stations and four rest stations (not very well staggered – most of us had four vivas in rapid succession somewhere in the sequence).

Viva 1 presented a 65-year-old lady with abdominal pain, nausea, lethargy, weakness and polyuria. The opening question was on ‘immediate management’, but led fairly promptly into differential diagnosis, where my top-of-the-list, hypercalcaemia, proved to be correct. Questions followed on causes of hypercalcaemia, investigations, management (including drug doses and mechanisms of action), types of hyperparathyroidism, and the interaction between calcium and phosphate, before the bell went.

Viva 2 concerned a three-week-old neonate who presented shocked and comatose; again, immediate management (including sizes of ETT, fluid doses, predicted weight, how to insert an intraosseous needle), differential diagnosis (the question never settled on a specific diagnosis, but we skimmed through different types of congenital heart disease and errors of metabolism as well as the more mundane sepsis or child abuse), investigations, initial ventilation settings, and retrieval logistics.

Viva 3 described a gentleman with extreme intra-operative hypertension, worse after IV beta-blockers – could only be phaeochromocytoma, though we went through the motions of a differential. After initial management, questions mainly focused on pharmacology of different antihypertensives (including MgSO4) and their relevance to phaeo.

Viva 4 was a sad tale of an alcoholic epileptic found unconscious in a pool of vomit in his hostel room. Yet again, differential diagnosis (where do you stop?!), initial management, and then several questions on delirium: definition, prognostic significance, prevalence in ICU, and management.

Viva 5 presented an elderly gentleman with an acute abdomen, new-onset AF and a past history of a cancer laparotomy. It followed the familiar course of immediate management, differential diagnosis, then reaction to deteriorating physiology, post-op management, ending up with a refractory coagulopathy; the bell went just as we got into the meaty territory of Recombinant Factor VIIa (I should have been quicker!)

Viva 6 concerned a gentleman admitted to ICU electively after pneumonectomy: he looked great in the initial scenario, and questions focused on pre-op prediction of post-op difficulties, and management of his chest drains. How would I respond when a few hours later he suddenly collapsed with hypotension and hypoxia? Turned out to be due to pulmonary haemorrhage – then how would I manage his broncho-pleural fistula after re-operation?

All-in-all the vivas seemed fair. All were clinical (no stats, EBM or managerial-type questions), most followed a predictable pattern, and all were on fairly everyday ICU problems (OK, phaeochromocytoma and hypercalcaemia aren’t exactly everyday problems, but they’re pretty much set pieces for an exam). In sharp contrast to my UK (DICM) exam, there seemed to be little or no requirement to be familiar with current ICU literature: only once was I asked if I was aware of any evidence to support my position (in choice of tranquiliser for delirium), whereas the UK examiners wanted a reference for just about every third sentence. My examiners were generally pretty neutral; two gave encouraging smiles and ‘well dones’, and one was very slightly 'hawkish'.

The vivas finished shortly after midday; by about 2.30pm the results were out, handed out to us in sealed envelopes. About 70% of us passed (a bit higher than the running average), including at least two UK DICM graduates. The unlucky few slipped away quietly; the remainder lined up to shake the hands of a long line of examiners and share a congratulatory drink or two, before departing to contemplate a life suddenly relieved of a vast amount of pressure!