Table of Contents

Though a distinction is being made between diabetic ketoacidosis and HONK, the two really form a part of the same disease spectrum. Some ketoacidosis is present in HONK, and some hyperosmolarity is present in DKA. However, different mechanisms are at play. HONK is distinct form DKA, and the distinction is not entirely arbitrary, at least from the management point of view. For instance, even though the conditions co-exist 30% of the time, it is possible to treat pure HONK without any supplemental insulin (because there is a satisfactory amount of it in circulation already).DKA is 3 times more common, but HONK has 3 times greater mortality. The chapter on DKA presents a table of discriminating features to help distinguish HONK from DKA.

Positioned on the end of the ETT, the capnograph should be able to pick up the expired carbon dioxide (EtCO₂ ) in whatever  gas happens to be wafting past it, and this concentration is recorded on a graph. This is plotted as a very useful waveform. The pattern of CO₂ concentration over time has features which give us some information about the gas movement in the airways and in the alveoli. These features, though they have no standardised names, are well recognised, and sometimes crop up in the fellowship exams as questions demanding certain waveforms to be graphed.

LITFL has an excellent synopsis of the current BTF guidelines, which is a well-referenced revision resource. The BTF guidelines also form the basis of the summary detailed below.  An extensive rambling discussion of these recommendations is also available at the end of this chapter, but it  has diminished relevance in the context of pre-exam panic. Links to discussions with greater detail are made available for those who are interested. Specific SAQs interrogating this topic consist of Question 15 from the first paper of 2013; however there are numerous questions which inidrectly address this issue by asking about the management of raised intracranial pressure.

The college loves to include "define this" or "calculate that" questions in the exam paper, largely because the definitions of statistics terminology are usually quite fixed, not open to interpretation, and therefore easy to grade (i.e. you either get zero or you get full marks). The only exception was the ancient Question 2b from the first paper of 2001, which asked  "What is the relevance of Evidence Based Medicine to your patients and how will you apply this?" which is equivalent to asking a high school English class to write essays on the topic of "What does freedom mean to me?". Fortunately, this sort of thing has not been seen for a while. Even raw definitions of such pleb items as sensitivity and specificity have not been seen since about 2008 (i.e they disappeared around the same time as the CICM Part I appeared on the scene; this primary exam then seems to have absorbed many of the EBM definition questions). These days, Part II tends to feature "fellow-level" questions about interpreting funnel plots and examining meta-analysis articles for validity.

These equations are important, because the questions upon which they are bases are rather binary. Either you get it right, in which case you get full marks, or you get it wrong, in which case you get nothing. This is an important concept to internalise, as there is nothing better than easy marks earned by the mindless rote-learning of equations. Commit these equations to memory. Ideally, on the day before the exam. This part of the training program has the poorest cortical retention rate; one must walk to the written Part II venue very slowly and carefully so that this information doesn't fall out on the way from the train station.

Therapeutic and prophylactic hypothermia are effective methods of controlling number-induced panic in the depressing setting of severe traumatic brain injury. To some extent ICP is regulated by the cerebral metabolic rate, and metabolic rate is affected by temperature: ergo, with the reduction of temperature one should be able to reduce the ICP. There are also seductive theoretical benefits, suspected influence on the cellular damage, inflammation,  oxidative injury, etc. More importantly, the intensivist feels better. With control of temperature comes a reduction in the ICP, and the anxiety-provoking monitor begins to display more pleasing values. Also, the use of muscle relaxant to reduce shivering has a calming effect on the nursing staff (a paralysed sedated patient is easy to look after). However, there may be no benefit in this technique as far as patient-centered outcomes are concerned

This is a summary of the physiological responses to the total or near-total absence of nutrition. In brief, the metabolic response to starvation is characterised by a switch from carbohydrate metabolism to fat metabolism, in the context of a hypometabolic state, with minimised catabolism. Initially, stores of carbohydrate precursors (eg. glycogen) are depleted. Then, in the first 24-48 hours there is increased gluconeogenesis from amino acids and glycerol. Subsequently, ketogenesis takes over, and much of the body metabolic needs are met by ketone bodies and free fatty acids. This is the consequence of decreasing insulin levels, and relatively increased influence from catecholamines and cortisol. Over prolonged starvation, protein catabolism begins, resulting in degradation of structurally important proteins, and organ system dysfunction.

Dyssynchrony is the effect of the patients respiratory demands not being appropriately met by the ventilator. The patient has their own idea about how to breathe, and the machinery supporting them, instead of making breathing easier, interferes with respiration and increases the work of breathing. Patient-ventilator dyssynchrony has occasionally appeared in the past papers.  Question 11 from the second paper of 2001 discussed the topic in a broad "what is it and what's your management" sort of way. On the other hand,  Question 21 from the first paper of 2007 was weird - it discussed the reasons for apparent triggering in a brain-dead patient, which  is a dyssynchrony of a sort, as it represents inappropriate auto-triggering by the ventilator.

Question 3.1 from the first paper of 2009 and Question 14  from the first paper of 2002 asked about Wolff- Parkinson-White syndrome. Specific issues asked about have included the characteristic ECG findings (short PR and delta waves), contraindicated drugs (AV nodal blockers like digoxin), and complications (SVT and sudden cardiac death). In brief, that's all you need to know. But of course many people (among them college examiners) would not be satisfied with a single sentence answer.  To address the issues of WPW in greater detail, one may need to refer to published literature. If one were pressed for time, one may safely limit one's reading to the LITFL page on WPW. If one were for some reason in need of greater detail, one might instead read the  UpToDate chapter on WPW.

Bioavailability is the fraction of the dose which reaches systemic circulation intact. IV bioavailability is by definition 100%. "Absolute" bioavailability compares one non-IV route with IV administration, and "relative" bioavailability compares one non-IV route or formulation with another (instead of using IV route as a reference). Bioavailability is measured using the area under the concentration-time curve; according to Dost's Law the ratio of AUCs is the bioavailability value. 

This topic keeps coming up in the SAQs. One notable appearance was in Question 5 from the first paper of 2010, where the candidates needed to not only identify the features, but also the causes of the partial spinal cord injury syndrome. The canonical resource for this would have to be Ch.78 from Oh's Manual, Spinal injuries by Sumesh Arora and Oliver J Flower. Specifically, on page 798, cord syndromes are discussed with enough detail to pass Question 5. If one happens to not own the Manual, one may find a similar amount of detail in the "International standards for neurological and functional classification of spinal cord injury" from 1997, and in a similar article on classifying partial cord syndromes from 2000. And if one were for some reason in need of a massive amount of detail, one might instead wish to purchase a copy of Diseases of the Spine and Spinal Cord By Thomas N. Byrne, which remains a definitive text on this subject.

Before allowing the gentle reader to proceed, I should mention that specifically for the CICM trainees there is in fact an Official Blood Gas Diagnostic Sequence, promoted by Oh's Manual. This sequence is the nearest thing to a gold standard for blood gas interpretation and should probably be used to answer all those ABG-related CICM Fellowship SAQs.

As they sit in the fridge marinading in their own filthy excretions, human erythrocytes mutate into something grotesque, no longer resembling human blood and wholly incapable of carrying oxygen. It is unbelievable that anybody should want to infuse such material into their patients, and concerns have been raised about the safety of using particularly old cells as their near their expiry. In Australia, packed red blood cells can only be stored for a maximum of 42 days (which is slightly conservative - internationally, the maximum PRBC shelf life is 49 days). Surprisingly, international clinical trial data supports the safety of existing practice. CICM SAQs mention storage lesions often, but only Question 29.1 from the first paper of 2010 has actually asked anything directly about them.

Question 24.3 from the first paper of 2009 asks the candidate to list three causes of massive splenomegaly. This was a sub-question worth perhaps 3 of the 10 marks, in a 300-mark paper. A perfect answer would have only scored a maximum 1% in the SAQs, or 0.3% to the total of the fellowship exam outcome. It is therefore almost completely meaningless, and the savvy candidate will limit their revision of this topic to the short list of causes, ignoring virtually everything else.