I had little insight/foresight of how the weather would shape up for the following year in which this column would go to press. As I typed this in the final days of 2010 huddled over a key board, my mitten-clad fingers typed feverishly to keep myself warm. Outside, a deathly silence signalling that once again the world had ground to a halt because of the weather and the particular flocculent nature of the snow. It is a truism increasingly acknowledged that the subzero temperatures will preface a spike in the number of samples from primary care deemed to have pseudohyperkalaemia as a result of the down-regulation of the sodium–potassium pump. But colleagues in the emergency department will have much more serious concerns than factitiously aberrant biochemistry results. In addition to the increase in admissions for fractures and breaks of bones, sprains and strains of muscles comes the increased risk of frostbite, and the further north one is the greater the risk. So it was somewhat timely that a December issue of the BMJ featured an article on frostbite in its clinical review series (BMJ 2010;341:1151–56). It will have been of scant interest to the commuters in the home counties stranded overnight during the worst of the Arctic conditions on the train to nowhere – save as fuel for fires. However, one can never prepare too early for the return of the Ice Age so the cellular mechanism for the damage might be of interest to our August readership. Tissue injury occurs after the formation of ice crystals in the extracellular space with a consequent increase in extracellular oncotic pressure. There is then diffusion of water out of the cells as a homeostatic mechanism, which produces a disturbance in intracellular electrolyte concentration. As the tissues rewarm, the extracellular crystals melt causing tissue oedema. Specialist advice in managing remote – as in deepest Kent – cases of frostbite is readily available with the advent of mobile phone networks and the Internet and will improve diagnosis and treatment. Sophisticated imaging using technetium-99 will predict outcome in severe cases of frostbite.
Could I suggest as recreational reading for the emergency medicine practitioner Wilderness and Environmental Medicine (impact factor 0.747), the house journal of the eponymous Wilderness Medical Society. The September issue has a number of fairly hair-raising papers for the couch potato – the rewarming rate after snow burial or the medication of choice for treating high altitude headache. There is correspondence on the benefits or otherwise of medicinal alcohol for exercise-induced hyponatraemia (Wilderness and Environmental Medicine 2010;21:278–9). Frontline treatment for this is normally vigorous hypertonic saline fluid replacement, but the practicalities of performing this in the wilderness environment are difficult. Since the primary pathophysiological mechanism is thought to be an inappropriate increase in ADH, the article suggests ethanol as a practical alternative treatment. Why? Because ethanol – as anyone nursing a hang-over will verify – suppresses the release of ADH. Yup that parched dry feeling the morning after.
On a similarly alcoholic theme, the endgame series (aimed at readers preparing for postgraduate examinations) features a salutary case report (BMJ 2009;339:813). The subject was a seaman airlifted off a fishing boat initially complaining of loss of vision. He admitted to drinking home-made vodka and became increasingly more confused and his condition deteriorated further, necessitating transfer to a large urban emergency department. Methanol poisoning was considered the most likely explanation for the presenting symptoms. Determination of blood gases is a key investigation together with measurement of blood methanol or a proxy thereof such as the osmolal gap. The patient had a pH of 6.6 and a base deficit of 20 mmol/L. The serum methanol was 2100 mg/L. Unfortunately, the late presentation of the patient to medical attention precluded successful intervention with antidotes such as ethanol or fomepizole.
As the demographic of the readership judders relentlessly towards pensionable years, the life-prolonging benefits of having, as a nonagenarian, a down-regulated thyroid axis have been evaluated (JCEM 2010;95:4979–84). Earlier studies by the same gerontologist researchers raised the likelihood of low thyroid function as a heritable phenotype which could contribute to longevity of life. Low thyroid function was described biochemically as low FT4 and FT3 along with a tendency towards higher TSH levels. The authors speculate that the lower activity of the thyroid hormone axis serves as a mechanism to shift energy expenditure from growth and proliferation to protective maintenance. However, it is not known how down-regulated the axis is allowed to drop while still keeping us warm in winters such as we have just had.
And finally we have some more understanding of why amiodarone treatment can be associated with elevated TSH (Endocrinology 2010;151:5961–70). Using murine animal models, amiodarone and its main metabolite desethylamiodarone were shown to non-competitively inhibit the Type 2 deiodinase gene. This disruption of the deiodination pathway could result in the transduction of the T4 signal generating less T3 and thus modulating the negative feedback mechanism on the pituitary with a compensatory increase in TSH.
