Question 1a and Question 1b from the first paper of 2000 asks the candidate to discuss the management priorities in a patient with a spinal injury and a sensory level around C4-5. Important sources used for this topic include Ch.78 from Oh's Manual (Spinal injuries by S. Arora and O.J. Flower), Management of Acute Traumatic Spinal Cord Injury (2015) and Critical care of spinal cord injury (2001). The latter article, though it is over 15 years old, is a gold mine of information, and is the major reference for most of the material presented below. A synthesis of the all the sources was attempted, and rendered into what was supposed to be a brief summary, and turned into a shockingly long table.
The College, in their model answer to Question 1 from the second paper of 2014, have constructed an excellent resuscitation protocol, which does not afford this author very much room for improvement.One can merely summarise their model, and expand upon it with references. To be clear, this approach is not "Early Goal-Directed Therapy". Protocolised sepsis management may not be especially effective in reducing mortality (ProCESS, ARISE). Rather than a protocol, this is a stepwise method to tailor a bespoke response to septic shock for individual patients, which branches from simple to advanced management options.
A hiccup, or singultus, or synchronous diaphragmatic flutter, is a myoclonic spasm of the diaphragm, which is stimulated by the phrehnic nerve. The signal to hiccup is sent from the nucleus tractus solitarius. This issue has come up once, and only once, in Question 15 from the first paper of 2001.
This has come up in Question 2 from the second paper of 2014. Apart from neurosurgical options the College wanted their candidates to discuss blood pressure management, therapeutic hypothermia, likely prognosis and quality of life issues. Judging from the model answer, some detailed knowledge of the published trial evidence was expected. A section of Oh's manual is dedicated to this exact issue. Chapter 51 ("Acute cerebrovascular complications") by Bernard Riley and Thearina de Beer contains within it a few paragraphs on decompressive craniectomy, on page 571. It would be worth pointing out that the key issues raised in these paragraphs were also raised in the model answer, and one would be well advised to review this material in order to produce an answer which appeases the examiners. For all we know, Riley or de Beer wrote that SAQ.
The topic of massive ischaemic stroke has been explored by the College in Question 2 from the second paper of 2014, where the family of a patient with a malignant MCA stroke syndrome are asking about the utility of a decompressive craniectomy for MMCAS. That topic is large enough to merit its own summary. Acute supportive management of stroke is also asked about in Question 13 from the second paper of 2011 and Question 26 from the second paper of 2006. Overall, it is a popular area for discussion.
The question of what to do with the patient who has presented within 4 hours of having a cerebral infarct is brought up inQuestion 22 from the first paper of 2013, "A 60-year-old male presents 2 hours after the onset of vertigo and loss of consciousness. CT brain is performed and shows right basilar and vertebral occlusion with no evidence of infarction. Discuss two possible definitive treatment strategies for this condition, including the indications and contra-indications of each."
A number of factors inﬂuence the actual eﬀective serum concentration of an antibiotic administered to a patient with critical illness. An excellent article by Marta Ulldemolins (2011) goes though this very thoroughly. This issue has come up in Question 3.2 from the second paper of 2014. The candidates were expected to interpret a time-concentration graph representing two situations: one in which a steady concentration is maintained, and one in which there is drug accumulation and increased halflife due to ineffective clearance mechanisms. A more general question was asked in Question 1 from the first paper of 2000.
This is relevant for Question 9.1from the second paper of 2008, where the college asked about the mechanics of measuring pH, pO2 and pCO2. The candidates were expected to submerge deeply into the physics and chemistry of ion-selective electrodes.
This chapter is a short list of reasons as to why your ABG measurement may be wrong, i.e. not reflective of what is happening in the patient. In 99% of cases, it is a problem with the collection storage and transport of the sample, because these are factors which are subject to human input and thus human error. The self-calibrating blood gas analyser is a dutiful and dependable servant; some sort of failure in its internal workings will only rarely contribute to the error (and usually it will be because some idiot human has improperly calibrated it). Lastly, a tiny fraction of errors are begot by the physicochemical limitations of the measurement method (eg. when an absurdly high bromine concentration interferes with chloride measurement and returns a spuriously raised chloride concentration value).
For blood gas interpretation, there is an official "Diagnostic Sequence" available in Oh's Manual. It is presented in T.J. Morgan's chapter for Oh's Manual (Chapter 92, "Acid base balance and disorders"); an owner of the Manual may find it on page 943 of the 7th edition. One expects that the college examiners, being the authors of the Manual, expect their exam candidates to use this ritualised approach. Therefore, one deviates from it at their peril. However some people may find it possible, or perhaps even desirable, to modify this Diagnostic Sequence.
The college examiners seem to love nothing more than to throw seemingly normal-looking ABG results at the candidates, with the respiratory acidosis disguised by the effects of pregnancy. There are several such examples:
The interpretation of blood gas data relies on certain standard variables being in place. Apart from atmospheric pressure (which everybody always assumes is 760 mmHg), theother most important variable is temperature. Temperature changes the physicochemical properties of water, influencing solubility of gases and the autoionisation of water into H3O+ and OH-.
The reaction which creates H3O+ and OH- is an endothermic reaction. Therefore, as heat is removed from the system by cooling, the reaction is driven to the left (i.e. in the direction of reassociation) - thereby reducing the concentration of H3O+ and raising the pH. Increasing the heat in the system lowers the pH. In short, the pH of any given solution will change in a fairly linear association with temperature.
The principles governing the behaviour of gases in solution are fundamental to the understanding of gas exchange and gas transport in the blood. The major topics of this chapter are Dalton's and Henry's Laws, and the influence of temperature on the solubility of gases in body fluids.