{"id":34,"date":"2013-04-29T10:42:00","date_gmt":"2013-04-29T10:42:00","guid":{"rendered":"https:\/\/psychresidentresource.org\/?p=34"},"modified":"2013-04-29T10:42:00","modified_gmt":"2013-04-29T10:42:00","slug":"delirium-tremens","status":"publish","type":"post","link":"https:\/\/psychresidentresource.org\/?p=34","title":{"rendered":"DELIRIUM TREMENS"},"content":{"rendered":"
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<\/b>by Lida Prypchan<\/b><\/p>\n

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Delirium tremens was identified as a clinical syndrome by Sutton (an English doctor) in 1813, but he was unaware of its alcoholic nature.  It was Rayer, in 1819, who gave a new and excellent description of this delirium and insisted upon its alcoholic etiology.<\/span><\/div>\n

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Delirium tremens is the most serious of the complications of chronic alcoholism; although it only develops in chronic drinkers, it is not necessarily a complication of chronic alcoholism, since not all drinkers end up victims to it even though they run the risk of this.  The concurrence of certain somatic factors is first necessary before it presents an appearance.  This is observed exclusively in individuals who present organic lesions resulting from extreme abuse of alcohol over a period of from seven to ten years.  It is characterized by oneiric delirium with typical symptomatology and certain physical symptoms among which the most significant are psychomotor agitation and trembling.<\/span><\/div>\n

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A few decades ago it was only noticed among persons from the lower classes, but for some time since then cases have also been observed in the upper classes, as well as among women, which was formerly the exception other than among prostitutes.<\/span><\/div>\n

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The age at which it occurs is generally between thirty and fifty.<\/span><\/div>\n

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Sudden deprivation of alcohol (abstinence) is very rarely the cause of D.T.<\/span><\/div>\n

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Constitutional predisposition toward alcoholism has been rejected as a significant factor leading to the appearance of D.T. because of the preponderance of people suffering from cyclothymic delirium, which should not be interpreted in the sense that the manic-depressive constitution predisposes one to D.T., if not to alcoholic habits.  Normally it is not usual to find psychopathic or psychotic deficiencies among those suffering from D.T., only that they are individuals of vigorous mental and physical health, whose natural robustness has resisted their alcoholic excesses for years.<\/span><\/div>\n

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D.T. is due to certain metabolic alterations which increase the toxins in the central nervous system, or prevent their destruction.  Some authors focus on hepatic insufficiency as a decisive factor in the production of these toxins; others, on the other hand, refer to renal insufficiency and yet others to cardiac insufficiency.  What is certain is that general pathogenesis cannot be inferred but the almost invariable presence of hepatic lesions speaks in favor of a single pathogenesis of metabolic origin.<\/span><\/div>\n

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Its presence is announced by various premonitory symptoms, the most significant being sleep disorders: short, restless sleep, appearance of terrifying nightmares.  It may also be preceded by one or more epileptiform crises, which can initiate an epileptic fit.  Preceded by these symptoms or appearing completely unannounced, acute alcoholic delirium occurs suddenly in the overwhelming majority of cases.  The clinical pattern is so typical, that it hardly ever presents any difficulties in diagnosis, and is characterized by somatic and psychic symptoms.  The first somatic symptom to come to attention is the excessive trembling during any movement of the limbs, mainly the hands and tongue.  The second is the profuse sweat running down the face.  The third is persistent insomnia, so the individual can rest neither by day nor by night.  Temperature is an essential indicator.  It reaches 39-40\u00b0C in two or three days, jumping around then remaining there for several days.  There is a tendency to believe that there is no such thing as apyretic D.T.  The initial fever of 40-41\u00b0C indicates acute hyperazotemic alcoholic delirium.<\/span><\/div>\n

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The psychic symptoms are: hallucinations, balance disorders, professional delusions, receptive functions, mental derangement, emotional and behavioral disturbances.<\/span><\/div>\n

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Hallucinations are the most striking symptom of delirium, consisting mainly of highly varied and haphazard visual and tactile (rarely auditory) hallucinations.  The visions are multiple, kaleidoscopic, scenic and microptic, relating to swarms of animals, talking birds, assassins armed with knives, legions of soldiers or dwarfs.  Those who suffer from haptic hallucinations experience hairy, threadlike sensations, water dripping, they feel animals biting or insects stinging, or their whole body itches.  In auditory hallucinations sounds are manifested, but these are more typically rhythmic noises like monotonous singing. By combining hallucinations from the different senses, the subject can see representations of the most diverse scenes: nocturnal processions of witches and dead people singing funeral songs, sounds of bells, a huge fair with puppet shows and fantastic circuses.  They may also experience kinetic sensations, flying off to a witches\u2019 Sabbath, falling over a waterfall or off a tower, or getting out of bed and rising up into space.<\/span><\/div>\n

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The course, symptomatology and duration of each episode of acute alcoholic delirium cannot be described diagrammatically because of its severity and the variety of forms which it takes.  The length varies from two to eight days; some cases may be fatal, but generally the attack ends with a long dream after an intense display of the above symptoms.  During its course, relapses may occur, or it could go into a sub-acute state, or continue into residual delirium.  Recovery is usually swift, but once the delirium has occurred, a certain predisposition toward recurrence remains.  When the delirium is over, the symptoms of chronic alcoholism continue. <\/span><\/div>\n

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by Lida Prypchan Delirium tremens was identified as a clinical syndrome by Sutton (an English doctor) in 1813, but he was unaware of its alcoholic nature.  It was Rayer, in 1819, who gave a new and excellent description of this delirium and insisted upon its alcoholic etiology. Delirium tremens is the most serious of the … <\/p>\n

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