With the implementation of pharmaceutical care as a clear responsibility of the pharmacist, the use of formal consult notes is increasing dramatically. Consult notes are designed to logically and succinctly outline and support a pharmacotherapy recommendation and to provide a record of the recommendation. Because it leads to clearer communication, can improve patient care, and because documentation is a key to successful reimbursement, you should become familiar with writing a consult note.There a few different ways to format the consult note, but almost all follow the SOAP approach to patient assessment. First you should identify subjective and objective information about the patient which is pertinent to the assessment of the drug-related problem, then assess the information, and finally offer a plan of action. Two examples follow.
As much as possible you should seek out primary literature to support your answer and, of course, cite that literature in the consult note. Your recommendations should be as specific as possible, e.g. avoid statements such as "monitor renal function." Identify what parameters need to be monitored, how often to monitor them, what the therapeutic goals are, and what to do if therapeutic goals are not achieved or toxicity occurs. Whether or not the written consult note is placed in the patient's chart depends on the rules of the facility in which you are working. The note may be given to the lead clinician if it is not possible to place it in the chart.
9/13/9041 yo WF admitted with 2-week hx of fatigue, and one-week hx of blurred vision and dizziness likely due to phenytoin toxicity (admit serum conc 49.6mcg/ml; usual therapeutic range 10-20 mcg/ml). Wt 57.5 kg, allergies: NKDA. Meds PTA include: phenytoin 100 mg. po qAM, 200 mg po qPM; mephobarbital 32mg po qAM, 64mg po qPM; prochlorperazine 25mg PR q12h or 10 mg po q6h prn; 5FU 1000 mg IV on 8/14, 5FU 500mg IV on 9/6, leucovoran 30mg IV on 9/6. The pt states she has been taking her medications "as usual" (no capsules taken above required dose) and denies use of any OTC medications or other non-prescribed drugs.
A review of the literature found no likely drug interactions could have accounted for the increase in phenytoin serum concentrations with the possible exception of the prochlorperazine, for which one paper noted that on one instance it seemed to "impair" phenytoin metabolism (JAMA 1968;203:969). Since no other information was given regarding the patient, extent of metabolism impairment, disease status, or concomitant medications/diseases, it is impossible to evaluate the likelihood of prochlorperazine causing an increase in this patient's phenytoin concentrations.
Phenytoin pharmacokinetics are non-linear and rise rapidly when hepatic metabolism is saturated by increased drug or decreased liver function. Given the timing of the chemo medications, we feel it likely that the chemo has inactivated enough of her metabolizing cells (P450 enzyme system), to decrease clearance and account for the increase in phenytoin serum concentrations.
We recommend continuing to hold the phenytoin, measuring serum concentrations every other day, until the concentration falls below 15mcg/ml, then reinstate phenytoin therapy at 100mg po qHS. Target serum phenytoin concentrations: 10-20mcg/ml. Measure serum concentrations in AM at 3 days and 7 days after initiation of new dose, then weekly while on chemotherapy regimen and monthly thereafter if she is doing well. Measure mephobarbital concentrations now (compare to last known serum concentration), and at one week after initiation of new phenytoin dose. This patient should be interviewed daily until phenytoin concentrations are stabilized at new dose. Interview to determine amount of dizziness/blurred vision, amount of N/V, and check for nystagmus or ataxia. If subjective signs/symptoms continue to occur at 100mg po qHS, then decrease dose to 30mg po qHS.
Thank you for the opportunity to evaluate this interesting patient.
Pharmacist Signature Here
Brief patient description goes here.I.M.A. Patient is a 40 year old white male with a history of drug abuse.Reasons for Consult
The Pharmacotherapy Consult Service was contacted because of increasing liver enzymes despite discontinuing carbamazepine and haloperidol.Information
Subjective & objective data go here, and you may refer to a graph, table, etc.
Mr. Patient's serum transaminases have been steadily rising even after discontinuing carbamazepine (Tegretol®) and haloperidol (Haldol®) therapy.He is currently taking:
- Lithium Citrate 900 mg/ day
- Lorazepam 1 mg t.i.d.
Pharmacotherapy Summary
What does the information tell you.
Several factors suggest a hepatitis B infection.
- The hepatitis screen indicates Hepatitis Cab as reactive, IgM non-reactive, IgG reactive, and Anti HBc reactive. HBSag is non-reactive possibly indicating non-recovery from active infection.
- The serum transaminases, AST (SGOT) and ALT (SGPT), are both elevated, and they are both greater than the alkaline phosphatase levels; while these indicators are non-specific, they suggest a chronic active hepatitis infection.
- Several of the WBC counts were slightly higher than normal as were the neutrophils, lymphocytes, monocytes, and the eosinophil differential which may indicate a inflammatory condition and/or a viral infection.
- The serum total protein levels were in the high normal to slightly elevated range possibly indicating host mediated immunoactivity.
- Mr. Patient's history of drug abuse may indicate a source of the hepatitis B virus.
- The serum transaminases, AST and ALT if elevated by carbamazepine hepatotoxicity would not increase upon discontinuation the drug.
- The high haloperidol levels on 9/1 and 11/5/96 may indicate an inflammatory liver condition which could inhibit the normal metabolism of haloperidol thus causing a rise in the serum levels.
Recommendations
- Treat Mr. Patient for hepatitis B by supportive therapy: bed rest, avoidance of strenuous physical exertion, alcohol and hepatotoxic drugs.
- Continue to monitor Mr. Patient's transaminase levels, WBC with differential, and for any physical signs or symptoms.
- Carbamazepine is a known hepatotoxin and probably should be avoided (certainly during the acute phase of the hepatitis) unless it has had a very clear beneficial effect.
- If it is clear he has responded historically well to haloperidol, it can be carefully re-instated. Haloperidol is reported to increase liver enzymes, but so do most of the other antipsychotics agents. There is currently no reason to believe haloperidol is the cause of the increased liver enzymes seen in this patient. Successful doses may be lower than that used recently to treat Mr. Patient.
- We are currently awaiting more information from a literature search about this subject.
Thank you! We would be happy to help you follow this interesting patient.
Pharmacist Signature Here
Date
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Stanley S. Weber, Pharm.D, FASHP, BCPP Director, Joint Doctor of Pharmacy Degree Program University of Washington and Washington State University Copyright © 1998 Comments: expharmd@u.washington.edu
Revised: June 24, 1998