Signs and symptoms associated with hypoglycemia include nervousness, diaphoresis, weakness, light-headedness, confusion, paresthesia, irritability, headache, hunger, tachycardia, and changes in speech, hearing, or vision. Acidosis results from uncontrolled diabetes mellitus, with hyperpnea (Kussmaul respirations) as the outstanding symptom. The hallmark symptoms of hyperglycemia are increased thirst, fruity breath, and glycosuria. The signs and symptoms of diabetic ketoacidosis include Kussmaul respirations, fruity breath, tachycardia, abdominal pain, nausea, vomiting, headache, thirst, dry skin, and dehydration.
Dietary deficiencies judged by a body mass index less than two standard deviations below normal, a history of grossly impaired dietary intake, or an abnormal thiamine assay. Cerebellar dysfunction, including ataxia, past pointing, dysdiadokinesia, or impaired heel-shin testing. Altered mental status or mild memory impairment, judged as inability to recall two or more items in the four-item memory test or impairment on more elaborate neuropsychological tests of memory function. If untreated, signs and symptoms may progress to unconsciousness, seizures, coma, and death. Annual economic loss in the United States alone, related to poor job performance and absenteeism associated with hangovers, is thought to be $148 billion, with light-to-moderate drinkers contributing the major share.75 Although a strict definition is lacking, headache, diarrhea, anorexia, vomiting, tremulousness, and fatigue are commonly recognized symptoms. Though a few isolated cases of anaphylactic reactions have been reported, IV administration is the preferred route of administration in the ED.108 The ocular findings of Wernicke?s syndrome may resolve within hours, but other deficits may require days, and recovery may be incomplete.
It is not unexpected that many such patients seek emergency medical care; likewise, the history of recent alcohol use may not be readily offered. There have been concerns that the administration of hypertonic dextrose to patients without thiamine administration could precipitate Wernicke?s encephalopathy.109 For this reason, it has generally been recommended that thiamine be given before hypertonic dextrose.
A recent comprehensive review containing little hard evidence suggested that rehydration, prostaglandin inhibitors (non-steroidal antiinflammatory agents), and vitamin B6 may represent effective therapy.76Ethanol WithdrawalAlcohol withdrawal syndrome develops 6-24 hours after a decrease in ethanol intake and lasts from 2-7 days.
However, the evidence for this is weak, based on poorly described case reports where the patients involved either had prolonged dextrose without further nutritional support or had evidence of early Wernicke?s encephalopathy before they received the dextrose.Following the initial dose, thiamine should be continued on a daily basis along with additional supportive measures including IV fluids, repletion of potassium and magnesium, and maintaining adequate glucose levels. Some patients experience mild symptoms of irritability and sleeplessness, while others suffer major withdrawal characterized by fever, diaphoresis, and hallucinations. Most patients experience autonomic hyperactivity with tremulousness, sweating, nausea, vomiting, and agitation.77 Vital signs reflect an elevation in heart rate and blood pressure. These bags of IV fluids, hanging solicitously over the alcoholic, generally contain a concoction of thiamine, folate, multivitamins, and magnesium. Generalized seizures (alcohol withdrawal seizures) result from neuronal excitation and can occur within 12-24 hours of abstinence, as discussed in the next section.The most dramatic presentation of alcohol withdrawal is delirium tremens (DTs), characterized by auditory and visual hallucinations, confusion, disorientation, and pronounced autonomic hyperactivity.


A recent review questions the value of this practice.110 The authors argue that single IV doses of these elements are not likely to reverse a long-standing deficiency and point out that there is no direct evidence linking hypomagnesemia to alcohol withdrawal, as is commonly believed.
It may be confused with metabolic disorders (such as hypoxia, hypoglycemia, hyperthyroidism, and hepatic encephalopathy) or with infectious disasters (such as sepsis, meningitis, or encephalitis). While routine administration of thiamine to all alcoholics may again be ?overkill,? toxicity is unlikely. While it may be given by mouth, intramuscularly, or intravenously, the IV route is best suited for the patient in moderate to severe withdrawal. Begin with 2-5 mg lorazepam followed by repeat doses of 2- 5 mg every 20 minutes as needed to control symptoms.When using benzodiazepines, avoid switching agents but instead administer repeated doses of a single agent.
The decision to admit may involve both medical factors (such as vital signs, neurologic examination, and response to therapy) as well as social considerations (including family support, a place to stay, money for medication, and the like).
Alcohol detoxification units may be suitable for those who have stable vital signs and are not hallucinating or confused.Withdrawal SeizuresAlcohol withdrawal seizures usually occur between 12 and 24 hours from the cessation of alcohol intake.
While patients may have other signs of withdrawal, seizures may be an isolated phenomenon unaccompanied by a hyper-adrenergic state.Do patients with alcohol withdrawal seizures need a CT scan of their head? They were randomly assigned to receive either 2 mg of lorazepam or normal saline intravenously and then observed for six hours.
Only 3 of 100 patients (3%) who received lorazepam had a second seizure, as compared with 21 of 86 patients (24%) in the placebo group.
When even small amounts of alcohol are consumed in the presence of disulfiram, an unpleasant reaction?consisting of flushing, headache, nausea, vomiting, vertigo, abdominal discomfort, palpitations, and diaphoresis?occurs.
When ethanol is consumed and metabolized, the resultant acetaldehyde accumulates, causing the classic ?disulfiram-alcohol reaction.?91 The symptoms begin as soon as five minutes after ingestion, peak at 15-20 minutes, and may last hours. The intensity of the reaction varies from person to person but in general is proportional to the dose of both alcohol and disulfiram. There is a striking ?rash??a moderate-to-intense erythema of the face, proximal upper extremities, and torso?that can be part of the disulfiram-ethanol reaction.
Theoretically, metoclopramide should be avoided because of its antagonist properties, which may worsen existing hypotension. It begins with a decrease in carbohydrate intake with resultant depletion of glycogen stores. As free fatty acids are utilized, ketoacids are formed.The initial symptoms are anorexia and nausea, followed by protracted vomiting and diffuse abdominal pain. These symptoms further reduce oral intake, and a downward spiral begins.Clinical EvaluationOn examination, most patients show signs of volume depletion, including tachycardia and orthostatic hypotension.


Unless there is a co-existing problem such as sepsis or hypoglycemia, mental status is usually normal. The diagnosis is generally made with the help of an electrolyte panel, which will demonstrate a wide anion gap acidosis. A blood gas (either venous or arterial) is not absolutely necessary in classic presentations, but a serum pH can help determine the severity of the acidosis. A double disorder occurs when persistent vomiting adds a metabolic alkalosis to the underlying ketoacidosis. A triple disorder occurs when these two phenomena are compounded by a respiratory alkalosis associated with withdrawal.
Ketones are present in both the blood and urine of these patients, although not always in measurable form. Routine laboratory tests rely on the nitroprusside reaction, which is sensitive for acetoacetate and acetone but not for ?-hydroxybutyrate.
It has a low mortality rate, and when death does occurs, it is generally attributed to coexisting disorders.93,95 Clinical response is the best way to follow the patient?s response to intervention.
Isotonic fluid resuscitation will normalize volume status and promotes renal excretion of both ?-hydroxybutyrate and acetoacetate.95 Glucose stimulates endogenous insulin and reduces further ketone production. When saline alone was compared to the combination of saline and glucose, the patients who received both therapies resolved their acidosis more quickly.96Potassium and magnesium stores should be repleted, and thiamine administration is advisable.
Bicarbonate administration is not indicated in the management of AKA, because correction of the acidosis occurs rapidly once volume is restored and glucose is administered.94,95 DispositionMost patients will resolve their dehydration and acidosis within 8-12 hours.
In one series, almost half of patients (46%) did not require admission.93 Patients with AKA may be well-suited for management in short-term observation units in the ED. Criteria for discharge from the ED may include an anion gap that is headed toward normal (15 or so), resolution of the acidemia, normal hydration, and the ability to tolerate oral fluids. Of those who survive, recovery is often incomplete, with significant long-term morbidity.103ED EvaluationThe triad of Wernicke?s encephalopathy consists of oculomotor disturbances (classically, ocular palsies and nystagmus), altered mental status, and ataxia.



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