The traditional approach to AWS symptoms has been to sub-divide the illness into "mild," "moderate," and "severe" manifestations, which are said to emerge in a relatively predictable sequence, beginning with mild. This may have been a reasonable approach given the limited understanding of the brain at the time it was adopted, but there was never much research behind it. The basis was a study with only 10 participants conducted at the Lexington, KY federal narcotics hospital in the late 1940s. All patients studied were male, relatively young, and relatively healthy.
Pharmacology for AWS has generally focused on sedatives. Over the years, as truly "old-style" treatments such as chloral hydrate, phenobarbital, and alcohol drip fell into (very appropriate) disfavor, benzodiazepines such as Librium and Valium advanced to the head of the class. Thus, the treatment of choice for all severe AWS symptoms became benzodiazepines.
What's wrong with this picture? Well, if you are treating patients who are only minimally ill and do not have major co-morbidities, perhaps nothing.
But if you are dealing with more severe and prolonged withdrawal in a patient population with serious medical problems (alcohol-related or not), it can pose real problems. For example, let us imagine a patient with underlying mild alcoholic dementia who is also suffering from mental status changes due to alcohol withdrawal. If such a patient is given benzodizepines, the likely result is a worsening of the symptoms — mental confusion plus underlying cognitive dysfunction. In this case, sedatives will not lead to a more alert and aware patient, and may in fact make confusion worse. This has not been appreciated as a major problem because confusion in this setting is always attributed to AWS! In fact, if a clinician follows a protocol based on a defined dosage schedule without reference to symptoms, the eventual results may include behavioral disinhibition, violence, a fall or other accident, or at the extreme (and we have seen this numerous times) a comatose patient in the ICU.
Our approach has these foundations:
In our manual, we divide AWS signs and symptoms into Types A, B, and C. Type A symptoms are related to CNS excitation, and include anxiety, a sense of foreboding, and a hypersensitivity to light and sound. Type B symptoms are hyperadrenergic, and include elevated blood pressure, tachycardia, tremor, and sweats. Type C comprises AWS-related delirium. (Looking at the Type Indicator© will give you a quick overview.)
We have found that these symptoms occur quite independently of each other, and may appear in almost any variety of sequences and combinations.
To give a concrete example, older patients tend to be less sensitive to hyperadrenergic effects and are more likely to have underlying cognitive deficits (including those associated with a long history of alcoholism). As a result, they may manifest a sudden mental status change (Type C) as their first and sometimes only significant AWS symptom (for example, as a post-surgical patient). If the clinician is expecting the "classic sequence" of mild, then moderate, then severe withdrawal, the diagnosis of AWS may initially be missed.
The division of symptoms into clusters A, B, and C is not arbitrary. Not only does each cluster share a common probable pathophysiology, they also tend to respond best to particular classes of agents. Benzodiazepines, if not otherwise contraindicated, may in fact be a good choice for Type A symptoms, although we have also used agents such as DepakoteTM to good effect. For Type B symptoms, the priority is clearly to counteract the hyperadrenergic symptoms. Our manual recommends a variety of anti-hypertensive agents. For Type C symptoms, low doses of neuroleptics combined with supportive care are generally indicated. And please, since there are numerous cautions, contraindications, and special circumstances, read the manual for more detail.
Note also that the classes of agents we recommend for each symptom cluster are drugs that one would generally give to non-AWS patients experiencing the same symptoms. In fact, we think it's a very good reality check to ask yourself this question:
"If this patient had symptom x and was not experiencing AWS, would I select this agent?"
Asking this question will help you to avoid many clinical misadventures, such as trying to control tachycardia and hypertension with benzodiazepines or other sedatives, a course which can lead to severe over-sedation and respiratory compromise.
Patients with AWS do not suddenly develop a radically different physiology. It is usually best to control their symptoms in the same general way you would control them in a non-AWS patient.
Benzos for hypertension?
While it is important to select the right agents for treatment, it is just as important to base treatment on the response to previous treatment.
We will give an example that cost a drug company a great deal of money, as in millions of dollars. Company X had a promising new anti-hypertensive agent and secured a patent for its use in AWS treatment. Unfortunately, their clinical trials featured a rigid pre-set dosing regimen. Their results? Horribly inconsistent.
In a few cases, hypertension was not sufficiently controlled. Some patients achieved excellent control of their symptoms. And more than a few patients developed severe hypotension.
Why? Well, the answer is simple: because the drug was being given without reference to the severity of symptoms (or even whether hypertension was present), some patients didn't get enough of the drug, some got just the right amount, and some got way too much. AWS patients often vary widely in their symptoms and response to treatment (more on that in a minute).
The conclusion Company X reached was that their new drug yielded inconsistent results and should not be used in AWS treatment.
If Company X had based their treatment on the presence or absence of symptoms (in other words on response to treatment) rather than on a pre-set regimen, they almost certainly would have found that their drug was in fact effective for AWS treatment. Being good guys, we actually called them up and tried to explain this to one of their executives, who didn't want to hear about it. (And yes, if you are reading this and work for a drug company, we are willing to play ball as long as what you are proposing represents good patient care.)
As our story about hypertension and hypotension illustrates, AWS patients vary widely in their expression of symptoms and their response to treatment.
These differences can be based on co-morbidities, individual physiology, age, degree of addiction and tolerance, and (it sometimes seems) the phase of the moon. This variability has given AWS the reputation of being a difficult and vexing condition to treat. As a nursing friend of ours once put it, the problem with following a set treatment plan for AWS is that the patients don't always follow the plan!
Feedback from the patient is the most important item to consider in making treatment decisions.
When we designed our treatment system, we took the variability of AWS as a given. The system had to work the same way regardless of the symptoms present, their severity, or their order of presentation. It also had to work despite wide variations in response to treatment.
In our system, you evaluate symptoms, treat with appropriate agents, monitor response to treatment and then adjust treatment based on the response. It doesn't matter if patient A and patient B are manifesting completely different symptoms. Following the system will "automagically" lead to treatment tailored to each patient's individual symptoms.
Since the monotherapy model has been around for so long, we find that as soon as you mention anything other than benzos in AWS treatment, many people assume (naturally enough) that you are suggesting monotherapy with a new and different drug: valproic acid, or clonidine, or beta-blockers. This is definitely not what we are suggesting. In our system, you treat only the symptoms present, and treat them with agents which are appropriate for those symptom types (following the Type Indicator©).
To clinicians accustomed to benzodiazepine monotherapy, our system at first seems extremely complicated: three different symptom groups, three different classes of drugs, and no comforting progression of symptoms. However, it's really much simpler than conventional treatment: you evaluate the presence or absence of symptoms, administer appropriate agents for those symptoms, evaluate response to treatment, adjust treatment as needed. After that, as they say on the shampoo bottle, it's just "lather, rinse, repeat."
How is this simpler? Well, for one thing it won't lead you to treat symptoms with an inappropriate agent, leading to unpredictable and sometimes unfortunate results. The Type Indicator© is extremely simple to administer and gives unambiguous results — no rating things on a scale of zero to seven. And because treatment is based on the presence or absence of symptoms, you don't have to hold any complex theories about AWS in your head (or communicate them to other staff members). The presence or absence of symptoms will tell you how the treatment is working, and what treatment is required now. Simply glancing at the completed Type Indicator© will give you (or any member of your staff) a very good idea of how the patient is responding.
Medical Disclaimer
All material on this website is for informational purposes only. Readers are encouraged to confirm the information contained herein with other sources. Patients and consumers should review the information carefully with their professional health care provider. The information is not intended to replace medical advice offered by physicians. The authors will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.