Show the model answerAttempt it first — that is what makes it stick
What earns the marks10 marks
| (a) What it is, then the numbers | 2 marks. A brief description of the pattern, then the count against percentage receptor blockade |
|---|---|
| (a) Get the direction right | Count 0 is 100% blockade. Writing that a count of 4 means over 95% inverts the whole relationship |
| (b) An example with every indication | 3 marks. The majority listed indications and gave no examples. The example is half the mark |
| (c) Two conditions, not one | 5 marks. The disadvantages must be tied to age AND to chronic kidney disease, not to suxamethonium in general |
| (c) The dose does not change | The single most dangerous error on this paper. mg/kg is unchanged in the elderly |
| (c) Do not write the background | The physiology of ageing, the stages of CKD, the mechanism of suxamethonium and the phases of block all scored zero |
| (c) The commonly forgotten four | Anaphylaxis, malignant hyperthermia, masseter spasm and suxamethonium apnoea were omitted by many |
2 marks
The train-of-four pattern, and its relationship with receptor occupancy
Two marks: one for describing the pattern, one for the occupancy relationship. Write the relationship as a short table, in the direction the question asks for.
| Feature | Detail |
|---|---|
| Pattern | Four supramaximal stimuli of 0.1 ms delivered at 2 Hz, so the train takes 2 seconds |
| Current | Supramaximal, 60–80 mA, to be certain every fibre in the nerve is recruited |
| What is read | Two separate things — the count (how many of the four are present) and the ratio (the height of T4 against T1) |
| Why it is the working pattern | It needs no pre-paralysis baseline. Each train carries its own control in T1, which is what a single twitch cannot do |
| Why fade happens | Blockade of presynaptic nicotinic receptors reduces the mobilisation of acetylcholine, so successive responses in the train diminish. Fade is present in a non-depolarising block and absent in a phase I depolarising block |
| Receptor blockade | TOF count | T4:T1 ratio | Single twitch height |
|---|---|---|---|
| 70% | 4 | 1.0 | 100% |
| 75% | 4 | 0.75 | 95% |
| 80% | 4 | 0.5 | 80% |
| 90% | 4 | 0.25 | 50% |
| 95% | 3 | — | 25% |
| 97% | 2 | — | 15% |
| 99% | 1 | — | 5% |
| 100% | 0 | — | 0% |
Commonly lost: A number of candidates mixed up the percentages, writing that a count of 4 corresponds to more than 95% receptor blockade. That is the relationship exactly inverted: over 95% blockade is where the count is falling to three and below.
3 marks
Indications for train-of-four monitoring, with examples
The question asked for indications with relevant examples, and the majority gave no examples at all. Write the indication in one column and what the monitor actually shows in the other.
| Indication | The relevant example — what you look for |
|---|---|
| Monitoring the depth of blockade | A count of 1 to 2 is the usual working depth for abdominal surgery; a count of 0 with a post-tetanic count of 1 to 2 is a profound block for a laparoscopic case |
| Assessing readiness for intubation | Loss of the train-of-four response at the monitored muscle after an intubating dose. The airway muscles are blocked before the hand, so this is a conservative indicator |
| Deciding when to give a top-up | Reappearance of T2 or T3 during maintenance, indicating the block is lightening before the surgeon complains |
| Deciding whether reversal is possible, and with what | Neostigmine needs at least T2 visible; below that its ceiling defeats it. Sugammadex 2 mg/kg at T2, 4 mg/kg when only a post-tetanic response remains |
| Judging readiness for extubation | A train-of-four ratio of at least 0.9, measured objectively. Visual and tactile assessment underestimates the depth of block, and experienced observers routinely fail to identify a ratio below 0.70 by eye — so a count of four and an apparently sustained train prove nothing about the ratio |
| Measuring neuromuscular recovery | Following the ratio back towards 1.0 in recovery. Below 0.9 the pharynx is weak, upper oesophageal sphincter tone falls and swallowing is uncoordinated, causing misdirected swallows; at 0.7 the ventilatory response to isocapnic hypoxia is specifically blunted while the response to hypercapnia is unchanged |
| Differentiating the type of block | Fade present with post-tetanic facilitation indicates a non-depolarising or phase II block; no fade and no post-tetanic facilitation indicates a phase I depolarising block |
| Research | Quantifying onset, ED₉₅ and duration between agents, which is where the comparative figures in every textbook table come from |
Commonly lost: The majority gave no examples. An indication without its example is half an answer to a question that asked for both in the same sentence.
5 marks — half the question
Suxamethonium in an elderly patient with chronic kidney disease
Five marks, and they are not for a general list of suxamethonium's side effects. Every point has to be tied either to age or to the kidney, and the background reading earned nothing.
Where age and the kidney each enter the argument
Suxamethonium is hydrolysed by plasma cholinesterase before most of the dose ever reaches the junction. Duration is set by how much enzyme there is, not by renal clearance.
Two separate arguments, and the question names both patients
The age argument
Plasma cholinesterase activity falls with age, so the same dose is hydrolysed more slowly and the block lasts longer. Reduced muscle bulk also makes fasciculation and myalgia less pronounced.
The kidney argument
Renal failure is itself an acquired cause of reduced plasma cholinesterase activity, alongside pregnancy, liver disease, cardiac failure, thyrotoxicosis and malignancy. The two causes compound.
The conclusion to write
A longer block than expected, in a patient whose starting potassium may already be high and whose cardiac reserve is limited. Not accumulation of the drug — slower destruction of it.
| Disadvantage | The general effect | What age or the kidney adds |
|---|---|---|
| Credited by the examination | ||
| Prolonged duration | Duration depends on plasma cholinesterase activity | Activity falls with age, and renal failure is a recognised acquired cause of reduced activity. The two together prolong the block |
| Hyperkalaemia and arrhythmia | Depolarisation causes potassium efflux, and a small rise in serum potassium is expected in any normal subject | Renal failure does not cause an exaggerated potassium release in itself. The danger is the starting value: potassium may already be grossly deranged, so a normal rise lands on an abnormal baseline and provokes arrhythmia |
| Bradycardia and other arrhythmias | Muscarinic stimulation at the sinus node produces sinus or nodal bradycardia and ventricular arrhythmias, more severe after a second dose and preventable with atropine | Poorly tolerated where cardiac reserve is limited, and the elderly are more likely to be on a beta blocker or a calcium channel blocker |
| Raised intraocular pressure | Rises by about 10 mmHg for a few minutes, against a normal range of 10–15 mmHg. It matters in a perforated globe, and a concurrent induction agent offsets it | Relevant to the cataract and vitreoretinal surgery this age group presents for |
| Raised intracranial pressure | Credited by the examination alongside the intraocular and intragastric rises, as a consequence of fasciculation | Relevant where cerebrovascular disease coexists |
| Raised intragastric pressure | Rises by about 10 cmH₂O from fasciculation | Lower oesophageal sphincter tone rises at the same time, so barrier pressure is preserved and there is no increased risk of reflux |
| Myalgia | Commonest in young patients mobilising quickly after surgery | Less pronounced in the elderly because of reduced muscle bulk — the mark was awarded only where this qualification was made |
| Omitted by many candidates | ||
| Anaphylaxis | About twice as likely as with a non-depolariser, at roughly 1 in 10,000 administrations | Less well tolerated where cardiac and renal reserve are already limited |
| Malignant hyperthermia | Suxamethonium is a trigger alongside the volatile agents | Age does not remove the risk; a first exposure can follow many uneventful anaesthetics |
| Masseter spasm | May be the first sign of malignant hyperthermia, and can make laryngoscopy impossible | — |
| Suxamethonium apnoea | Prolonged block from reduced plasma cholinesterase activity, genetic or acquired | This is where the age and kidney arguments converge, and it deserves naming explicitly rather than being left implicit in “prolonged duration” |
Commonly lost: A small number wrongly stated that suxamethonium increases the risk of aspiration. Marks were awarded for the opposite point: the rise in intragastric pressure is negated by the simultaneous increase in lower oesophageal sphincter tone, so barrier pressure is maintained.
Commonly lost: Many omitted anaphylaxis, malignant hyperthermia, masseter spasm and suxamethonium apnoea altogether. Four named items, in one line each, in a five-mark section.
Writing it in the time you actually have
Half the marks are in part (c)
The split is 2, 3 and 5. Most candidates spend longest on the train-of-four, which is worth the least.
| Minutes | Part | What to write |
|---|---|---|
| 0–4 | (a) · 2 marks | Two lines on the pattern — four supramaximal 0.1 ms stimuli at 2 Hz, count and ratio read separately — then the occupancy table. Do not write an essay on fade |
| 4–9 | (b) · 3 marks | A two-column table. Eight indications, each with the finding beside it. The second column is what most candidates left blank |
| 9–17 | (c) · 5 marks | State up front that the dose in mg/kg is unchanged, then the prolonged block from reduced cholinesterase in both age and renal failure, then hyperkalaemia against an already-deranged baseline, then the pressure effects, then the four commonly omitted items |
| 17–18 | Check | Confirm nothing in part (c) is a general fact about suxamethonium that could have been written without reading the stem |