EFFECTS OF ALCOHOL AND DRUGS ON MANAGEMENT AND OUTCOME

The presence of alcohol significantly affects the initial management of trauma patients. Intoxicated patients are more likely to require intubation for airway control, intracranial pressure monitoring for neurological assessment, and more diagnostic tests such as CT scans to evaluate the abdomen.^5,6 Alcohol use may also increase the risk of death from serious injury. One study used data from more than 1 million drivers involved in a crash and controlled for the effects of variables such as safety belt use, vehicle deformation, speed, driver age, weather conditions, and vehicle weight, and found that intoxicated drivers were more than twice as likely to suffer serious injury or death compared with nondrinking drivers in a crash of equal severity.⁷

Patients with a history of chronic alcohol use are more likely to have underlying medical conditions such as cardiomyopathy, liver disease, malnutrition, osteoporosis, and immunosuppression. Acute, in addition to chronic, alcohol use may also affect outcome from trauma. Alcohol causes respiratory depression as well as vasodilatation that limits the ability to compensate for major blood loss. One study measured the amount of hemorrhage required to induce hypotension in dogs, and found that intoxication decreased this volume by one third.⁸ Acute alcohol intoxication has also been shown to be immunosuppressive. One study analyzed infectious complications in patients with penetrating abdominal trauma and hollow viscus injury.⁹ A blood alcohol concentration of 200 mg/dl or more was associated with a 2.6-fold increase in abdominal infectious complications, even after controlling for chronic use.

The effect of other drugs, alone or in combination with alcohol, has not been as rigorously studied. Heroin causes histamine release, which decreases systemic vascular resistance, and may potentiate the effect of blood loss. Cocaine, especially in its free-base form known as “crack,” has the opposite effect, and causes peripheral vasoconstriction, pupillary dilation, tachycardia, and hypertension. These effects may mask or mimic the sequelae of injury.

ALCOHOL AND INJURY RECIDIVISM

Traumatic injury is a recurrent disease, especially in patients with alcohol or drug use disorders.¹⁰ In a 5-year follow-up study of 263 alcohol intoxicated patients admitted to a level I trauma center, the readmission rate was 44%.¹¹ Although the mean age of the group was only 32 years, the injury-related mortality was 20%, with 70% of deaths attributed to continuing alcohol and other drug use. In a larger, more comprehensive study, over 27,000 patients discharged from a trauma center were followed using death certificate searches to detect postdischarge mortality. Patients who screened positive for an alcohol use disorder had a 35% injury-related mortality rate during the study period, which was significantly higher than patients who screened negative.¹²

WITHDRAWAL SYNDROMES: PROPHYLAXIS AND TREATMENT

Withdrawal is characterized by signs and symptoms that are the opposite of the pharmacologic effects of the drug involved. The four primary categories are alcohol, sedative hypnotics, opiates, and stimulants. The goals of prophylaxis and treatment of alcohol withdrawal syndromes are to minimize the risk of complications such as seizures, delirium tremens, and cardiovascular morbidity that occurs as a result of sympathetic overload.

Symptoms from cessation of short-acting drugs like alcohol may emerge within 24–48 hours, while withdrawal from long-acting drugs like chlordiazepoxide or methadone may not emerge for 3–5 days. Alcohol and sedative hypnotics have similar pharmacologic effects. Patients in the intensive care unit often receive benzodiazepines, leading to a delay in manifestations of alcohol withdrawal until after the patient is transferred to the floor. After 4 or 5 days it is no longer clear if symptoms should be attributable to alcohol or to benzodiazepine withdrawal, although treatment is similar.

Two main types of alcohol withdrawal prophylactic regimens exist. The first is symptom-triggered therapy, and the second is fixed-schedule dosing with a taper. Symptom-triggered therapy reduces the amount of medication administered, as many patients develop only mild symptoms that do not require therapy.¹³ Symptoms are measured using a questionnaire such as the Clinical Institute Withdrawal Assessment–Alcohol Revised short form (CIWA–Ar), which measures 10 signs and symptoms of alcohol withdrawal on a 0–7 scale (nausea, tremor, autonomic hyperactivity, anxiety, agitation, tactile, visual and auditory disturbances, headache, and disorientation).¹⁴ Treatment is titrated to maintain a score in the mild (8–10) range. Although the CIWA–Ar has been used in general medical settings, it requires training and experience, must be repeated at regular intervals, and is not feasible in critically injured patients. For these reasons, fixed-scheduled dosing is commonly practiced in most trauma intensive care units.

All currently existing guidelines recommend the use of benzodiazepines as a primary therapy for alcohol withdrawal.¹⁵ Agents with a short to moderate half-life such as lorazepam are often used when frequent neurological assessments are needed, but may require increased overall dosage and more frequent administration in comparison to the longer-acting benzodiazepines such as diazepam and chlorodiazapoxide. Longer-acting drugs are preferred because slow elimination provides an intrinsic tapering effect.

The administration of alcohol for prophylaxis, either intravenously or orally, is no longer considered acceptable. Alcohol may block some of the autonomic effects of withdrawal, but it lowers the seizure threshold, is difficult to titrate, is highly toxic to tissues in the event of extravazation, increases the risk of gastric mucosal bleeding, may increase liver transaminase levels, and may precipitate acute liver failure in critically ill patients with reduced hepatic reserve.

There is a role for adjunctive agents such as beta blockers, clonidine, and neuroleptics, but none of these should be considered as primary therapy, and they should not be started until adequate doses of benzodiazepines have been administered. These agents do not prevent withdrawal syndromes, and may increase the incidence of delirium tremens by selectively reducing autonomic manifestations and agitation, causing delayed recognition of worsening withdrawal.

The principles of preventing and treating sedative-hypnotic withdrawal are similar to those used for alcohol. Management consists of substituting short-acting agents for longer-acting ones, and tapering the dose by 20% per day over 5 days. Cessation of stimulant use such as cocaine or methamphetamine is characterized by symptoms of depression and a substantial risk of suicidal behavior due to depressed cerebral dopamine levels.

Patients with opiate dependence may experience flu-like symptoms as the dose is tapered. Withdrawal from opiates may also be delayed in onset due to appropriate use of analgesics in trauma patients. Opiate withdrawal is highly stressful, but is not usually dangerous, as symptoms are much less severe than those seen with alcohol or benzodiazepine withdrawal. However, attempts to wean addicts on chronic methadone maintenance are inappropriate in an acute care setting. Their dose should be considered as maintenance, and additional opiates provided as needed for pain.