Diabetic ketoacidosis is a state of insulin deficiency, characterised by rapid onset, extreme metabolic acidosis, a generally intact sensorium, and only mild hyperglycaemia. DKA comes up frequently in the CICM SAQs, but usually as an ABG interpretation exercise. This chapter focuses on the medical side of DKA, including its causes, manifestations, complications, and management strategies.
This is a summary of trials and guidelines related to metabolism nutrition and endocrinology, aimed at the CICM Part 2 exam candidate. The objective was to list the important studies, link to an authoritative analysis, and produce a pithy one-liner to help remember the main points.
Given that this is a common and practical ICU problem, the college have wisely included it among their SAQs - Question 10 from the second paper of 2008 asks the candidate to "Outline and justify your approach to “clearing” the cervical spine in an adult multi-trauma patient with a severe closed head injury". Other similar SAQs include Question 11 from the second paper of 2013 and Question 4 from the second paper of 2011. College answers to their own question are cut-and-pasted from The Alfred official evidence-based C-spine clearance protocol (2009).
Acute status asthmaticus is a fragile thing which, most ICU specialists would agree, is a good reason to get out of bed and drive to the hospital. These people tend to die rather readily, typically of cardiac arrest due to dynamic hyperinflation and the resulting loss of preload. This is made worse by the fact that the excellent outpatient management of asthma has filtered out the mild and moderate patient groups, and left only the incredibly brittle severe asthmatics. Only these are the people who ever get admitted to ICU for mechanical ventilation. Thankfully, even the ICU management of these people is improving, and in spite of an overall worsening severity of their illness, their ICU mortality has been steadily improving.
Transpulmonary pressure (TPP) is the difference between the alveolar pressure (Palv) and pleural pressure (Ppl), for which oesophageal pressure (Pes) is a reasonable surrogate. It is the net distending pressure on the lung parenchyma, and therefore should be the variable we use to adjust our ventilator settings. Unfortunately, it has several problems. You never know ehere the balloon is and what its really measuring, and when it measures something you never quite know whether that pressure is equal across the entire pleura. Also, it migrates. And there is only one RCT in support of this technique, which did not reach statistical significance with hard outcomes. But, it remains a fascinating physiological toy, and companies have been quick to adopty and market this device. You will see it soon in the well-funded private hospital near you.
Basic definitions of CRRT nomenclature (such as "what is the transmembrane pressure") has been asked about in Question 30 from the second paper of 2014 and Question 14 from the second paper of 2007, The best resource for such definitions seems to be the ADQI site, which (in the "ADQI Reports" section under "CRRT") has a "Definitions/nomenclature" workgroup statement. The definitions in this statement are used wherever possible in the following text.
Diuretics do not have a defined classification system in the same way as antiarrhmics may, but they do fall into discrete classes. Carbonic anhydrase inhibitors, loop diuretics, osmotic diuretics, aldosterone antagonists, thiazides and drugs acting on the vasopressin-aquaporin system have discrete and unique mechanisms of actions, and they generally do not overlap. This chapter tries to consolidate all of these substances into some sort of logical structure.
Broadly speaking, constipation is associated with inadequate nutrition due to pooor feed tolerance, delayed ventilator weaning and slower ICU progress, with some authors reporting an increased length of ICU stay and increased mortality. The therapy scales up from simple things (stopping the constipating drugs and mobilising the patient) all the way to neostigmine infusion and manual disimpaction.
There are situations in which vast quantities of IV heparin fail to increase the APTT in spite of your every effort. One might call this "heparin resistance", or "heparin insensitivity". For some reason, this issue seems to enjoy a significant amount of attention from the college. Particularly, Question 13.2 from the first paper of 2012, Question 8.1 from the first paper of 2011 and Question 6.2 from the second paper of 2008 all ask the candidate to give reasons as to why the patients APTT might be so low in spite of heparin therapy.
This is a fascinating topic, and one which has surprising amount of herpetology in it. A more indepth discussion of the reptilian contribution to coagulation tests is available elsewhere. Also, there is an excellent article which details a stepwise approach to the coagulopathic patient, and the manner in which the diagnosis of an isolated coagulation abnormality should be approached. An even greater depth of explanation (and more detailed references) can be found at Practical-Haemostasis.com.
An agonist is a ligand that binds to a receptor and alters the receptor state resulting in a biological response. A full agonist reaches the maximal response capability of the system, and a partial agonist does not (even at full receptor occupancy). A partial agonist acts as an antagonist in the presence of a full agonist (if they compete for the same receptors). An inverse agonist is a ligand that by binding to receptors reduces the fraction of them in an active conformation. Spare receptors are said to exist wherever a full agonist can cause a maximum response when occupying only a fraction of the total receptor population.
This is a summary of the factors which determine neurological outcome after cardiac arrest. It has been assembled from the college model answers to the many questions they always seem to ask about this topic (it is very popular with the SAQ writers), as well as using the most recent ERC/ESICM statement (Sandroni et al, 2014)