TCA’s in the Elderly – Which One Should We Use and When?

TCA’s in the elderly are generally discouraged especially for symptoms of sleep and depression.  There are a lot of other options to consider for treatment of both of these issues before TCA’s.  While I’m not going to tell you what is ALWAYS right or wrong in using TCA’s in the elderly, I’m going to share with you a scenario that I’ve seen in my practice.

85 year old female with a history of depression is currently receiving Elavil (amitriptyline) 10 mg daily.  Her depressive symptoms have responded significantly from this medication.

We know Elavil is on the Beer’s list.  We know anticholinergics do not have a good side effect profile, especially in the elderly.  So what do we do?

A few questions that I’d be starting to think about:  Do we try to change it to another antidepressant?  Do we try a TCA like nortriptyline which may tend to have a better side effect profile in the elderly?  Do we know if she has tried anything else in the past?  Are there other symptoms involved (neuropathy etc.)?  Has she failed off this medication in the past?  Are there any potential side effects or indicators of the prescribing cascade (constipation meds, dry mouth, artificial tears, cognition issues, falls etc.)?

In a scenario like this, I’ve seen all of the above done.  I’ve seen changes to nortriptyline, SSRI’s, other antidepressants, and providers leaving it alone as well.  What’s the best strategy?  It is a tough call sometimes.  It is very important to work with patients (and their families if applicable), and get an excellent medical history to help assess the severity of the condition, potential side effects, possible safer alternatives as well as how much benefit that medication has brought to that patient.

Want more?  Check out the PDF I created – 30 medication mistakes that every healthcare professional should know!  It’s FREE.

Restarting ACE Inhibitors in CHF – Speaking From Experience

I think most of you who follow the blog know I spend most of my time dealing with polypharmacy and geriatrics.  I’m going to use the example of ACE Inhibitors in CHF to demonstrate my point.  Every now and then, I will see patients who have a history of CHF and are not on an ACE Inhibitor.

With issues of falls, low blood pressure, renal impairment, electrolyte imbalances and so on in the elderly, it is a tough decision sometimes whether or not to start or restart an ACE inhibitor.  For someone who has significant hypertension and no issues with falls, good kidney function, that decision to start an ACE inhibitor in CHF is certainly a little bit easier.

I do want to caution you about using ACE/ARB Inhibitors in CHF patients (and really any compelling indication for blood pressure medications).  The problem I’ve seen a handful of times particularly in our patients with long term CHF is that they may have been on an ACE/ARB before.  They may not have tolerated it in the past and if you ever come across a long term CHF patient, be very diligent in digging into their past history.

Courtesy Blausen.com staff
Courtesy Blausen.com staff

I once had a nursing home resident who was started on an ACE Inhibitor twice and it resulted in hyperkalemia twice.  What happened was this patient switched providers, and following the “guidelines” an ACE was added.

The major point I want you to take away is that if something seems fishy, be sure to thoroughly investigate the patient history if you are going to start a new medication or recommend starting a new medication.

Looking for more clinical pearls from the real world?  Check out the FREE PDF of 30 medication mistakes I see in my practice as a clinical pharmacist!

Goodpasture’s Syndrome

A 21 year old African American male patient with no pertinent medical history presented to the ED by EMS in pulseless electrical activity (PEA) cardiac arrest. As per family at bedside, patient had been having cough with no sputum, headache, fatigue, bloody diarrhea, some chest pain, shortness of breath, and signs of dehydration for the past 3-4 weeks. On the morning of presentation to ED, patient’s sister noticed that he had fallen on his way to the bathroom and began foaming at the mouth. After EMS responded, patient lost pulses en route to the ED. CPR was initiated, 3 rounds of epinephrine were given, and intubation occurred upon ED arrival. Urine toxicology screen was positive for marijuana and benzodiazepines. Patient was found to be in respiratory failure and bronchoscopy showed blood clots in bronchioles. Moreover, patient was in renal failure, resulting in a serological work-up to determine the cause.

Patient was given a total of 6 plasmapheresis sessions, and then continued on intermittent hemodialysis. The medical team following the patient, as well as renal and rheumatology consulting physicians had high suspicions for Goodpasture’s syndrome (GS). Anti-glomerular basement membrane (anti-GBM) antibodies were drawn, with the first two yielding weakly positive results.

GS is a rare organ-specific autoimmune disease that is mediated by anti-GBM antibodies. It typically presents as acute renal failure caused by a rapidly progressive glomerulonephritis, accompanied by pulmonary hemorrhage. The incidence of GS is estimated to be 1 case per million per year, but it is a cause of acute renal failure in approximately 20% of all cases of rapidly progressive or crescentic glomerulonephritis. The exact cause has not been able to be determined, however, certain respiratory infections may trigger the disease and exposure to hydrocarbon fumes, metallic dust, tobacco smoke, or substances such as cocaine may increase risk. Furthermore, symptoms could start out slowly, gradually affecting the lungs and the kidneys, or may become rapidly severe in a matter of days. Initial symptoms may include fatigue, weakness or lethargy, nausea and/or vomiting, loss of appetite, and pale appearance [1-2].

Diagnosis of GS is made through the detection of circulating anti-GBM antibodies; however, kidney biopsy provides definitive diagnosis. GBM antibodies detected by immunoassay have been reported to be highly specific for GS. The sensitivity of this test approaches 87% in untreated patients with systemic disease. A positive test for anti-GBM cannot be relied upon exclusively to establish the diagnosis. Weakly positive test results (5-30 EU/mL) may occur in other immune-mediated diseases, in patients who do not have anti-GBM antibody-mediated disease [3]. In this patient, of the four anti-GBM tests done, their highest positive titer was 2.1 (>1.0 AI: Antibody Detected), representing a weakly positive result.

As for treatment, the 3 principles of therapy in anti-GBM disease are to rapidly remove circulating antibody by plasmapheresis, to stop further production of antibodies using immunosuppression with medications, and to remove offending agents that may have initiated the antibody production. Standard therapy consists of the combination of high doses of glucocorticoids, cyclophosphamide and plasma-exchange, which are all what this patient received [1-2].

Ultimately, after a lengthy hospital stay, this patient’s condition improved. However, they were still reliant on hemodialysis. A renal biopsy was necessary, but patient kept rescheduling and refusing, therefore the patient was discharged with an appointment for follow-up in the rheumatology clinic. So was this a presentation of Goodpasture’s syndrome? Although their anti-GBM antibody was positive, titers were very low. GS is technically possible, but probably unlikely.  References

Submitted By: Chandni Dudhia, PharmD-PGY 1 Pharmacy Practice Resident in collaboration with Donna M. Lisi, PharmD, BCPS, BCPP, Barnabas Health Care System, South Plainfield, NJ

5 Dangerous Mistakes With Fentanyl Patches

In my practice as a clinical pharmacist, I see the use of fentanyl patches on pretty much a daily basis.  I’ve seen numerous mistakes with fentanyl patches and wanted to put together a list of 5 dangerous mistakes.  In no particular order:

1. Fentanyl patches are extremely potent.  Many healthcare professionals don’t realize how strong a fentanyl patch is.  Opioid conversions are never perfect, but conservatively, a total daily dose of oral morphine 45-60 mg is approximately equivalent to fentanyl 25 mcg patch.  Because of this, I’ve seen numerous cases of inappropriately high starting doses, especially in the elderly population.

2.  Lost or missing patches should scare you.  Fentanyl as mentioned above, is extremely potent.  There is significant risk of children/pets getting access to a used patch.  Take a lost or missing patch very seriously.  Simply do a google search of fentanyl patch deaths and you’ll understand what I’m talking about.  Flushing of used patches is recommended per ISMP.

3.  Fentanyl patches are meant for chronic pain.  I’ve seen orders numerous times for fentanyl patches from the ED or primary providers for the treatment of acute pain.  You are not helping patients relieve their acute pain.  With an onset of action that takes hours to days once applied, a patient can be in pain for a long period of time before the drug begins having an effect.

4.  Delayed withdrawal.  Fentanyl patches basically create a deposit of drug being slowly absorbed through the skin.  I remember a case where a patient was on a chronic higher dose (100 mcg) and the patch was discontinued in the ED without any follow up or supplemental opioids.  Long story short, they ended up having withdrawal symptoms, but not until hours after they were discharged.  (Remember slow onset as well as slow elimination and offset)

5.  Drug diversion.  Whether at home, or in healthcare settings, I’ve dealt with numerous cases of drug diversion.  These cases even go to the point of diverters removing used patches from dementia patients.

Looking for more real world clinical pearls?  Check out the 30 medication mistakes I see in my everyday practice as a clinical pharmacist – a free resource for subscribers.

Difficulty Breathing: What could be contributing?

75 year old African American female with history of chronic heart failure (CHF), hypertension, atrial fibrillation with an implantable cardioverter-defibrillator (ICD), diabetes mellitus, asthma with chronic obstructive pulmonary disease (COPD), came to the ED with a chief complaint of “I woke up this morning and could not breathe”. The patient also had a cough with thick yellow and green phlegm, wheezing, and chest congestion. The patient reported worsening of the symptoms over the past couple of months with several admissions during this time for similar symptoms. The patient was treated with one nitroglycerin 0.4 mg SL tablet, furosemide 80mg IV, placed on CPAP, and given 2 doses of albuterol-ipratropium 3 ml nebulizer prior to arrival by EMS resulting in some improvement in symptoms. While in the hospital, the patient was started on metoprolol 50 mg tablet oral BID, enalapril 5mg tablet oral daily, amiodarone 400 mg BID, albuterol-ipratropium 3 ml nebulize every 6 hours, and fluticasone-salmeterol 250 mcg-50 mcg 1 puff BID. Patient’s vitals on arrival were: BP= 100/63, HR= 70 and RR= 18. Her chest X-ray showed diffuse interstitial, slightly nodular, opacities bilaterally and pulmonary venous congestion consistent with that observed during prior admissions.

Patient’s shortness of breath was diagnosed as CHF exacerbation. However, it is important to examine the patient profile closely to find possible underlying/contributing cause(s) of the symptoms. The patient was started on amiodarone 400 mg BID as a loading dose a year and a half ago for paroxysmal atrial fibrillation with rapid ventricular response (RVR). Prior to beginning of amiodarone, cardioversion was attempted. The plan was to wean the dose of amiodarone to 200mg TID for 1 week and then 200mg BID. However, patient’s dose was not re-evaluated and was continued at 400 mg BID. In this case, one of the possible contributing factors to the patient’s worsening pulmonary function could be prolonged use of amiodarone at a high dose.

One of the most serious, potentially life threatening adverse reaction of amiodarone is pulmonary toxicity; it is one of the leading causes for discontinuation of the drug. Some of the common pulmonary manifestations of amiodarone-induced pulmonary toxicity (AIPT) are interstitial pneumonitis, organizing pneumonia, eosinophilic pneumonia, acute respiratory distress syndrome (ARDS), pulmonary fibrosis, diffuse alveolar hemorrhage, pleural effusion. Risk factors for AIPT are uncertain but, may include a high cumulative dose, daily dose greater than 400 mg/day, duration of therapy exceeding two months, increased patient age (> 60 years), pre-existing lung disease, thoracic or non-thoracic surgery, and pulmonary angiography. The prevalence of AIPT is estimated to be about 5-7%. Two major hypotheses of AIPT include a direct toxic injury to lung cells and an indirect immunologic reaction. Due to the frequency and potential severity of AIPT, early detection is desirable. Patients who may benefit from amiodarone should be carefully selected and the lowest effective dosage of amiodarone should be administered. Treatment of AIPT consists primarily of stopping amiodarone and, in most patients, initiating systemic glucocorticoids at the dose equivalent to oral prednisone 40 to 60 mg/day. Patients with mild symptoms (dyspnea on mild to moderate exertion) and normal oxygenation can be observed off amiodarone without glucocorticoids.  References

Submitted By:

Chandni Dudhia, PharmD-PGY 1 Pharmacy Practice Resident in collaboration with Donna M. Lisi, PharmD, BCPS, BCPP, Barnabas Health Care System, South Plainfield, NJ

Interprofessional Medication Education