Category Archives: Ambulatory

VA Ambulatory Report 12.13.17 – Flatulence!

Thanks to Vaibhav who presented his patient’s case of bothersome flatulence found to have positive celiac serologies, but negative EGD now being treated for H. Pylori.  This case allowed us to have an excellent discussion about approaching a less common chief complaint such as flatulence and how we diagnose celiac disease and IBS.

Learning Pearls    Screen Shot 2017-10-11 at 12.58.11 PM

  • Patients may experience belching (also called eructation), flatulence, or abdominal bloating due to decreased intestinal motility or increased sensitivity to normal gas production.  Reference the Rome IV criteria for diagnostic criteria of functional gastrointestinal disorders.
  • Healthy individuals are not able to completely digest some carbohydrates which leads to increased H2 production.  This is the basis for the H2 breath test for carbohydrate malabsorption
  • A low FODMAPs diet has good evidence for symptom reduction in patients with IBS. Some studies have shown benefit in other functional gastrointestinal disorders and in patients with IBD with symptoms such as bloating not explained by their inflammatory disease
  • Anti-TTG is testing for IgA antibodies and may be falsely negative in individuals with IgA deficency.  Consider co-testing with IgA levels or testing for Gliaden.  No test is perfect and the gold standard is small bowel biopsy.

 

More than you want to know about Intestinal gas

  • There is about 200 mL of gas in the intestinal system
  • The main elements in gas are nitrogen, oxygen, carbon dioxide, hydrogen, and methane
  • The odor in gas comes from minor elements such as methanethiol, dimethyl sulfide, hydrogen sulfide, short-chain fatty acids, skatoles, indoles, volatile amines, and ammonia.
  • Where does intestinal gas come from?
    • 1 – Swallowed air
    • 2 – Digestion of fat and protein leads to production of CO2 in the small bowel
    • 3 – Bacterial fermentation leads to production of Hydrogen and Methane
      • Hydrogen
        • Normal in the colon
        • Produced in the small bowel in SIBO
      • Methane
    • 4 – Carbohydrate malabsorption
      • In healthy individuals, foods with high concentrations of oligosaccharides (such as wheat, oats, potatoes, and corn, legumes) cannot be completely digested by enzymes within the normal small bowel, leading to increased H2 production
        • This increased colonic H2 production from carbohydrate ingestion is why we perform the H2 breath test for carbohydrate malabsorption
      • Fructose malabsorption may be an underappreciated cause of gastrointestinal symptoms. Up to one-half of the population cannot completely absorb the load of fructose consumed in the average diet
    • 5 – Diffusion from the blood
  • Gas Disorders (Look to the Rome IV criteria for diagnosing these conditions)
    • Belching (also called Eructition)
      • Involuntary belching occurs after meals
      • Can be increased by foods that decrease LES tone such as chocolate, fats, mints
      • Chronic, repetitive belching due to habitual air swallowing
    • Flatulence
      • May patients reporting bothersome flatulence produce a normal amount of gas but may be experiencing symptoms from it due to: alteration in intestinal motility or bacteria, dietary factors, or physiologic factors that heighten awareness of gas
    • Functional Abdominal Bloating and Distention
      • Correlation between symptoms of bloating and amount of gas production is inconsiente
      • Similar underlying contributors as flatulence: decreased gut motility, increased sensitivity to gas,
      • Rome IV criteria for diagnosis: recurrent bloating or distention at least on day/week and insufficient criteria for diagnosis of IBS, functional constipation, functional diarrhea, or postprandial distress syndrome

 

What is up with the FODMAPs diet?

  • FODMAPs = Fermentable, Oligo, Di, Monosaccharides and polyols
  • Studies have consistently shown improvement in symptoms on a low FODMAPs diet for patients with IBS including this recent RCT conducted in the US demonstrated a low FODMAP diet reduced IBS symptoms reduced symptoms
    • There is evidence it can be helpful in symptom reduction for other functional gastrointestinal disorders and in patients with IBD but symptoms such as bloating or discomfort that are not related to inflammatory disease
    • There is some evidence
  • Key concepts to teach to your patients
    • Elimination or limiting of all FODMAPs (not just one component)
    • FODMAPs foods are not the cause of the symptoms, but help reduce symptoms related to visceral hypersensitivity or decreased gut motility
  • Here is an excellent review article on FODMAPs

 

Diagnosing Celiac disease – why are Celiac Serologies so confusing?

  • When we check anti-TTG this is traditionally testing for IgA antibodies
  • Given the co-occurence with IgA deficiency, you may also want to test for IgA to ensure there is also not IgA deficiency leading to a false negative TTG
  • Gliaden is an IgG test and therefore avoids the problem with IgA testing
  • Gold standard is duodenal biopsy looking for
  • HLA testing is helpful in very specific instances (possibly in high probability population and discordance on serology and biopsy)
  • Remember, patients should be on a gluten-rich diet (yum!) when these tests are performed

 

What are the recommendations for “screening labs”

  • HIV: Screen in adults age 15-65 or at other ages if increased risk or pregnant
  • Screening for diabetes: USPSTF recommends screening in adults age 40-75 who are obese or overweight
  • Lipids: USPSTF recommends calculating ASCVD risk in all people 40-75
  • HBV, HCV: Screen in high risk individuals
  • No recommendations to get screening CBC, metabolic panel, or UA

Evernote link: https://www.evernote.com/l/AMrAvmVoGvRAdYlVY8T3cXx5RJIktWhm-Nw

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VA Ambulatory Report 11.28.17 – When your patient is seeing double – Diplopia and Stroke Pearls

Thanks Amanda for sharing your case of a middle aged male with a past history of diabetes and HTN presenting with diplopia found to have a sixth nerve palsy due to a pontine infarct.

Diplopia Pearls   Screen Shot 2017-10-11 at 12.58.11 PM

  • Your approach to diplopia should be the same as we approach any neurologic deficit –  Localize the lesion along the anatomic pathway
    • Central
    • Peripheral cranial nerve
      • Both a mononeuropathy or external compression of the cranial nerve
    • Extraocular muscles
    • neuromuscular junction
    • Globe (retina, cornea, lens)
  • Monocular diplopia vs. binocular diplopia
    • Binocular diplopia: If the diplopia is present only when both eyes are open then the diplopia is due to ocular misalignment
    • Monocular: Most often due to diseasse of the cornea or lens, less commonly the retina or cerebral lesion
  • Extraoccular muscle weakness can be subtle. LT pearl: when testing EOM, move your finger fast as this will be more likely to demonstrate subtle weakness than slow movements.
  • Cranial nerve palsies
    • 3rd nerve: longest cranial nerve after exiting the brainstem, more commonly affected by compression from an aneurysm or tumor.  When a third nerve palsy is due to microinfarction from diabetes it typically spares the pupil.  Therefore pupillary defects should raise your suspicion for intracranial lesion
    • 4th nerve: Most prone to injury from trauma and more rarely affected by microinfarction
    • 6th nerve: Most commonly affected

Check out this excellent chart from EB Medicine reviewing CN III, IV, and VI palsies.

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Stroke Pearls    Screen Shot 2017-10-11 at 12.58.11 PM

  • Code stroke: time sensitive interventions may be changing in the future
    • The latest trials are showing benefit to endovascular intervention in patients with large vessel occlusion within 6 hours of symptoms onset even after tPA administration.
    • Newer trials are investigating endovascular intervention up to 24 hours after symptom onset
  • Risk of future stroke after TIA: Use the ABCD2 score
    • This helps estimate the risk of stroke within the next 2 days after TIA
    • In patients with a risk < 1%, outpatient work-up may be appropriate
      • Goal is to get work=up completed within 24 hours

Evernote link: https://www.evernote.com/l/AMphZJl3GedO_Zz0p6Mjya3DIEWYfNB-uB8

VA Ambulatory Report 11.8.17 – Low back pain and spondylolisthesis

Thank you Kelly for presenting your patient with subacute worsening of chronic low back pain without red flag signs or symptoms found to have surprising findings on MRI of L3-L4 instability with spondylolithesis and edema causing mass effect on the spinal cord.

Screen Shot 2017-10-11 at 12.58.11 PM  Learning Pearls   Screen Shot 2017-10-11 at 12.58.11 PM

  • Don’t forget your physical exam maneuvers to assess for radiculopathy: straight leg raise (L4-S1); opposite straight leg raise (L5-S1); and reverse straight leg raise (L3-L4).
  • Order spinal MRI for patients with red flag signs or symptoms, pain that is progressive, or when it will change treatment (including referral for spinal injections or surgery)
  • Inflammatory markers may be helpful in determining who needs an urgent MRI

 

 

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The Physical Exam Maneuvers for the evaluation of Low Back Pain

  • Straight leg raise:
    • How to do: Patient supine, examiner raises affected side leg keeping it straight up to 60 degrees
      • Positive test: reproduces pain on side of leg raised
      • Suggests L4-S1 nerve root pain if radiates below the knee
      • Sensitivity = 80%, specificity = 40%
  • Reverse Straight Leg Raise (femoral stretch test)
    • How to do: Patient lying prone passively extending the hip and leg straight up off the plane of the table
    • Suggests L3 nerve root pathology if pain radiates into the anterior thigh
  • Opposite Straight leg raise
    • How to do: Patient supine, raise opposite side leg, keeping it straight
    • Positive if pain reproduced on the affected side
    • More specific test for L5-S1 radiculopathy
    • An L5-S1 radiculopathy is 95% sensitive for lumbar disk herniation (thus, the absence of radiculopathy almost rules-out a herniated disk)
  • FABERE (Flexion, Abduction, External Rotation, and Extension)
    • Consider performing if evaluating for hip or SI joint as cause of pain
    • How to do: Hip is externally rotated with the ipsilateral knee flexed at 90 degrees and placed on the opposite knee. Then apply downward pressure on the leg towards the examine table. Goal of getting leg parallel to exam table
      • If pain: indicates SI joint disease
      • If limited ROM: indicates hip, SI, or iliopsoas spasm

 

When to get imaging for low back pain?

  • Red flag signs or symptoms
  • If low back pain is not improving after conservative management and the patient is a candidate for surgery or epidural spinal injections
  • Imaging choice
    • MRI is ideal
    • Can consider a CT if a patient cannot get an MRI
    • Xrays may be helpful to evaluate for compression fracture and degenerative changes

 

When should I order inflammatory markers?

  • Consider ordering if you are concerning about do not miss diagnoses including seronegative spondyloarthropathies, malignancy, or infection.
  • Check out this article on the use of a clinical decision support tool utilizing risk factors and ESR/CRP to evaluate for spinal epidural abscess
    • The bottom line: The use of a clinical decision guideline for patients presenting to the ED with low back pain involving risk factors and ESR/CRP to determine who should receive urgent MRI decreased the time to diagnosis of spinal epidural abscess and decreased the incidence of neurologic deficits at the time of diagnosis.

 

Check out the ACP guidelines on the treatments for chronic low back pain.

Click here for an Evernote on Low Back Pain

 

VA Ambulatory Report – Polyarthritis and Drug Induced Lupus

Case Summary: Thank you Alicia for presenting your clinic patient a 20 yo F with refractory epilepsy presenting with subacute migratory polyarthritis after starting Oxcarbazepine concerning for Drug-Induced Lupus on top of SLE.

 

PearlsScreen Shot 2017-10-11 at 12.58.11 PM.png

  • Patients with drug-resistant epilepsy should be seen at a specialized epilepsy center
  • Thanks Chris Sha for teaching us the top three causes of infectious polyarthritis: Disseminated Gonococcal disease, spirochetes, and viral (HIV, HBV)
  • Approach to arthritis: Consider basing it on number of joints and inflammatory vs. non-inflammatory
  • Differentiating drug-induced lupus from SLE is based on clinical picture and  laboratory findings.
  • Anti-TNF drugs are increasing in use and can cause an atypical presentation of drug induced lupus.

 

Drug-resistant epilepsy

  • No set definition, but has been proposed that drug-resistant epilepsy may be defined as failure of adequate trials of two antiseizure drug schedules (whether as monotherapies or in combination) to achieve sustained seizure freedom
  • Other forms of treatment may be considered; vagal nerve stimulation, surgery
  • If seizures are not controlled after 12 months, the patient should be referred to a specialized epilepsy center
  • Ambulatory EEG monitoring?
    • More cost effective than in-hospital EEG. Can increase the yield of detecting a seizure due to longer time on monitors and patient’s are less sleep deprived when sleeping in their normal environment.
    • Gold standard for differentiating non-epilieptic seizures from epileptic seizures is still in-patient EEG.

 

Flashback to Katie Auriemma’s post on an approach to polyarthritis from the Moffitt Pearls earlier this week.

Drug-induced lupus (DIL)

  • Common meds: procanamide, hydralazine, penicillamine, INH
    • Also seen with TNF-alpha inibitors
      • Can be more atypically presentation of DIL including negative anti-histone antibodies, hypocomplementemia positive dsDNA antibodies
  • More often causes superficial lupus symptoms (joint pain, rash) over visceral involvement (anemia, nephritis, serositis, etc)
  • Diagnosis
    • History of taking a known offending medication
    • Development of one feature of lupus
    • Serology: Positive ANA.
      • Positive anti-histone antibody is strongly suggestive.
        • Can be seen in idiopathic SLE but those patients will also have positive subserologies
      • You can also see a positive ANCA
    • Resolution of symptoms within weeks of stopping the offending agent

 

How do I differentiate between SLE and DIL? 

  SLE DIL
Clinical presentation Average age of onset 20 -30 y

More likely to affect African Americans than Caucasians

Female: Male 9:1

Average age of onset 50 -70 y

More likely to affect Caucasians than African Americans

Female: Male 1:1

Lab Findings ANA positive > 95%

Anti-histone antibodies in 50%

Anti-dsDNA in 80%

Low C3/ C4

 

ANA positive in > 95%

Anti-histone antibodies in > 95%

Anti-dsDNA can be present

Normal C3/C4

 

VA Ambulatory Report 10.4.17 – Nephrotic Syndrome

Thanks to Akshai for presenting an interesting case of a 41 yo F with subacute bilateral leg swelling found to have nephrotic syndrome in the process of being evaluated for the underlying cause.

 

Pearls

  • Proteinuria can be broken into 4 causes: Overflow, glomerular, tubular, post-renal
  • When concerned about a glomerular process use your clinical findings and UA to help you determine if the picture is more consistent with nephritic vs. nephrotic
  • Nephritic Syndrome is often diagnosed with lab tests whereas nephrotic syndrome usually needs a biopsy to confirm the underlying cause
  • Treatment of nephrotic syndrome: ACEi/ARB for proteinuria, loop diuretic and salt restriction for edema, statin if hyperlipidemia does not resolve, warfarin if thrombosis.

 

What is the usefulness of BNP for lower extremity edema?

  • Breathing Not Properly Study: In a patient presenting with dyspnea a BNP cut off of > 100 can be helpful in determining heart failure over pulmonary cause of dyspnea
  • The ACC/AHA 2017 Focused Update gives a Class I recommendation for measurement of BNP in patients presenting with dyspnea, to support a diagnosis or exclusion of HF.
  • No studies have looked at BNP in a patient presenting with lower extremity edema as a predictor for heart failure
  • Can be elevated for a variety of reasons:  renal failure, cirrhosis, sepsis, anemia, stroke, OSA, PE and more.

 

Causes of Proteinuria (Forgive my powerpoint nephron drawing!)

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Nephritic vs. Nephrotic?

Disease of the glomerulus can be nephrotic or nephritic.  Use your clinical findings and UA to help you differentiate.

  Clinical Findings UA and urine sediment Findings Histology Findings
Mild Nephritic Asymptomatic microscopic hematuria and proteinuria

Occassionally gross hematuria

RBCs, dysmorphic RBCs, RBC casts

Mild proteinuria

Inflammatory lesions in less than one half of glomeruli
Severe Nephritic Edema

HTN

Renal Insufficiency

RBCs, dysmorphic RBCs, RBC casts

Heavy Proteinuria (>1.5g/day)

Diffuse glomerular disease
Severe Nephrotic Hyperlipidemia

Edema

Thrombotic disease

Heavy proteinuria (oftenr >3.5g/day)

Few casts or cells

Varies based on underlying cause

 

Nephrotic Range Proteinuria work-up for the PCP:

  • Send ANA, A1c, HIV, RPR, and Hepatitis serologies.
  • Refer to renal for likely renal biopsy.
  • Renal biopsy is often needed in adults whereas children are often treated with empiric steroids for presumed minimal change disease.

 

Treatment of Nephrotic Syndrome

  • Proteinuria
    • The degree of proteinuria is a predictor of renal failure. Treatment can reduce progression.
    • ACEi/ARBs – BP effects are immediate but proteinuria effects can take days-weeks
  • Volume Overload:
    • Due to sodium retention (not oncotic pressure from protein loss)
    • Diuretics; Slow diuresis to prevent hypovolemia, start with loop diuretics but may also need thiazide diuretics
  • Hyperlipidemia
    • Often reverse when underlying cause is treated and reversed
    • Most patients will need statin
    • Dietary modification does not help
  • Hypercoagulability
    • More common in membranous nephropathy
    • If thrombosis, treat with warfarin
    • Unclear if prophylactic anticoagulation benefit outweighs risks, practice varies amongst nephrologists
  • Treat underlying cause if identified

VA Ambulatory Report 9.13.17 – Vitiligo, Hashimoto’s, and Pernicious Anemia

Thank you to Rabih for presenting this interested case of a young man presenting to clinic with fatigue, weight gain, hypopigmented skin lesions found to have pernicious anemia, hashimoto’s and possible vitiligo.

Key Learning Points

  • For skin hypopigmentation try to determine if there is complete depigmentation vs. hypopigmentation to narrow your differential
  • Decision to treat subclinical hypothyroidism is based on level of TSH elevation, age, CV risk factors, and symptoms
  • Consider pernicious anemia as a cause of B12 deficiency especially in patients with other autoimmune diseases

 

Hypopigmentation of the skin

  • First try to determine if it is complete depigmentation or hypopigmentation.  This can be difficult especially in lighter skin individuals.
    • Degpimentation
      • Vitiligo – most frequent cause of depigmentation
        • Loss of epidermal melanocytes
        • Etiology not known, but associated with autoimmune diseases
        • No racial or ethnic propensity but often causing more impact on darker skin individuals due to is being more disfiguring
      • Consider exposures to chemicals (such as those found in hair dyes, insecticides, adhesives) or meds (topical steroids, imatinib, pegylated interferon)
    • Hypopigmentation
      • Commonly seen after an inflammatory skin process
      • Infections – pityriasis versicolor, leprosy, syphilis, non-syphilis treponema, onchocerciasis
      • Atopic – pityriasis alba
      • Rheumatologic causes – scleroderma, discoid lupus
      • Acquired
        • idiopathic guttate hypomelanosis – seen with aging
        • progressive macular hypomelanosis – unknown cause, possibly related to infection, typically seen in young adults, more common in darker skin individuals
      • Nutritional deficiencies – B12, copper, iron, kwashiorkor
      • Endocrinopathies – hypopituitarism, Cushing syndrome,

 

Subclinical Hypothyroidism

  • Definition: Elevated TSH with Normal T4
    • Always recheck after 2-3 months given these are numbers are dynamic to confirm subclinical hypothyroidism
  • When should we treat subclinical hypothyroidism? Based on TSH level, age, symptoms, TPO antibody status, and CV risk factors
    • TSH >10
      • Treat all patients <70
      • For patients >70 only treat if symptoms are present or have +TPO antibody
    • TSH 7-10
      • If symptoms are present
      • If patient is <70 and has cardiac risk factors or has +TPO
        • Patients who are younger and have +TPO antibodies are more likely to progress to overt hypothyroidism
    • TSH 4-7 AND
      • Symptoms of hypothyroidism: consider 6 month trial of treatment but stop therapy is symptoms do not improve with treatment
  • See this discussion in NEJM for more review of subclinical hypothyroidism
  • Recent study in NEJM showed no benefit to treating subclinical hypothyroidism in adult s> 65 years

 

Pernicious Anemia Fun Facts

  • What is pernicious anemia? Anemia due to autoimmune atrophic gastritis.
    • Autoanitbodies to intrinsic factor and parietal cells –> Loss of parietal cell mass –> hypochlorhydria and inadequate production of intrinsic factor –> B12 malabsorption –> anemia
  • It is called pernicious anemia because when it was described patients symptoms would progress gradually over time without available treatment
  • Diagnosis
    • Macrocytic anemia, low B12
    • Autoantibodies to parietal cells and intrinsic factor
      • Antibodies to IF are specific but not sensitive
      • Antibodies to parietal cells have better sensitivity, but only ~80%
      • If high enough concern and negative antibodies, may need EGD with biopsy demonstrating atrophic gastritis in the gastric body
    • Can also check serum gastrin which will be elevated
  • 40% of patients will have autoimmune thyroid disease
  • There is a theory that H. pylori infection may trigger the autoimmune destruction of parietal cells. However patients with pernicious anemia are less likely than age matched controls to have h. pylori. Associated with H. pylori infection thought possibly due to active infection gradually replaced by an autoimmune process
  • Increased risk of gastric neuroendocrine tumors and adenocarcinoma

VA Ambulatory Report Pearls 9.6.17 – Drug Induced Liver Injury

LT Pearls from the daily ditty about bacterial meningitis

  • Listeria meningitis is the one cause of bacterial meningitis that can have a lymphocytic predominant pleocytosis
    • CSF findings in Listeria meningitis can range from 100% PMNs to 100% monocytes

Thank you to Colin for presenting a patient seen in liver clinic with a history of alcoholic cirrhosis who recently stopped drinking found to have hepatocellular injury likely due to Disulfiram.

Learning Pearls:

  • DILI can be due to many different medications. To help you narrow your list, focus on the pattern of injury (hepatocellular vs. cholestatic) and the time course (acute vs. chronic)
  • Disulfiram can cause an acute hepatocellular injury and should be used with caution and monitoring in patients with a cirrhosis
  • In patients with cirrhosis with thrombocytopenia without anemia consider other sites of Epo production such as in HCC
  • First line medication assisted treatment for alcohol use disorder include Naltrexone, Acamprosate, and Disulfiram. Choose a medication based on patient goals and side effect profile.

 

Drug Induced Liver Injury (DILI)

  • Presentation
    • Depending on the offending agent:
      • Can see acute (< 3 months) or chronic liver injury (>3 months) dependi
      • Can see hepatocellular injury or cholestatic injury
    • Symptoms can vary based on severity of injury and pattern of injury
      • Patients are often asymptomatic
      • Can have non-specific symptoms including nausea, malaise, anorexia,
      • Can also cause present with symptoms similar to other causes of acute or chronic liver injury such as jaundice, pruritus, dark urine, pale stools
    • Diagnosis
      • Clinical diagnosis which can be hard to make
        • Known offending medication started prior to laboratory abnormalities
        • Stopping the offending agent leads to improvement in liver injury
        • Negative work-up for other causes
          • Assessment of other causes should be guided by history, physical exam, labs
        • If still uncertain the patient may need a liver biopsy
  • Medications that can cause DILI
    • There are over 1000 known medications and supplements that can cause DILI
    • Most common: Acetaminophen followed by antibiotics
    • Use the pattern and time course of liver injury to help you narrow your list of offending agents
    • Great resource for medications and supplements that can cause liver injury by the NIH: https://livertox.nlm.nih.gov/index.html
  • Disulfiram induced liver injury
    • Seen within 2-12 weeks of starting Disulfiram
    • Disease severity can range from asymptomatic elevations in aminotransferases to acute liver failure and death
    • Can have immuno-allergenic fevers with fever, eosinophilia and rash
    • No hepatic dose adjustment for patients with liver failure but should be used with caution and should monitor for hepatotoxicity

 

Lab abnormalities in cirrhosis

  • Pearl from LT: In patients with cirrhosis who have a thrombocytopenia with a normal hemoglobin think about Epo production from sites other than bone marrow (such as in HCC)
  • The classic LFT pattern in patients with alcoholic cirrhosis of AST:ALT of >2 is often maintained when there is another acute insult not related to alcohol
    • There is a hypothesis that the AST:ALT ratio in alcoholic use is due to a deficiency of  pyridoxal 5′-phosphate in alcoholics, a cofactor for the enzymatic activity of ALT.  This may explain why the pattern is maintained when there is a separate liver insult.
  • Shoutout to Rabih for these awesome pearls about patterns of LFT abnormalities.

 

Medications for Alcohol Use Disorder (AUD)

Medication Mechanism of Action Adverse drug effects and contraindications Evidence Who should I use this in?
Oral Naltrexone Blocks of the mu-opioid receptor involved in the rewarding effects of drinking ADE:

Transaminitis

 

Contraindications:

ALT or AST > 150s

Use of Opiates

Reduces relapse to heavy drinking (See 1, 2)

 

Reduces alcohol consumption compared to placebo

Helpful in reducing the amount of alcohol

 

Less effective for abstinence

Depot Naltrexone (Vivitrol) Same as above, but long acting requiring monthly IM injection Same as above Decreased rate of heavy alcohol use

 

Increased the number of abstinent days

If covered by insurance and patient prefers long acting form
Acamprosate Acts at GABA and glutamate neutrotransmitters –> reduce symptoms of protracted abstinence Three times daily dosing

 

Safe to use in patients with liver failure

 

Renal dose adjustment required

 

Contraindicated in renal failure

Increased proportion of heavy drinkers who maintained abstinence in European study

 

Not demonstrated in these two US studies

Consider if the goal if abstinence and patient cannot tolerate other medication options
Disulfiram Inhibits aldehyde dehydrogenase –> accumulation of  acetaldehyde –> flushing, nausea, palpitations, headache  if alcohol is consumed Contraindicated in severe heart failure or CAD

 

Avoid in pregnant or nursing women

 

Monitor for hepatotoxicity

Most studies have shown it to be no more effective than placebo in maintaining abstinence, but may reduce drinking days

 

Most effective when given in monitored setting such as by spouse (27)

Patients highly motivated to have complete abstinence

 

Patients can use periodically for high risk social situations

Topiramate Acts at propionic acid, GABA and glutamate receptors SE: Cognitive impairment, weight loss, headache, depression.

 

Off label use

 

Titrate gradually over several weeks

Decreased consumption in patients with SUD, similar effect as naltrexone Off label use, second line medication
Gabapentin Structurally related to GABA SE: Sedation and dizziness

 

Abuse potential

Higher abstinence rates and decreased alcohol consumption in small trials Off label use, second line medication
Baclofen   SE: nausea, vertigo, sleepiness

 

Generally well tolerated

Mixed results Limited evidence of efficacy, off label use
Nalmefene Opioid antagonist SE: nausea, insomnia, fatigue, psychiatric symptoms

 

 

 

 

Taken as needed shown to reduce number of heavy drinking days Not available in the US
SSRIs Inhibits breakdown to serotonin   Reduced alcohol intake in patients with depression and alcohol use No efficacy demonstrated in patients without depression
Ondansetron 5-HT3 receptor antagonist SE: diarrhea, headache

 

QT-prolongation

Some demonstrated effectiveness in subgroups: early onset alcohol use and patients with specific genetic variant of 5-HT3 receptor Off label use, only demonstrated efficacy in sub-groups

 

The VA has lots of resources for patients with substance use disorders including: PES, Addiction consult, OTOP, and inpatient rehab.

Check out the California Society of Addiction Medicine’s guide for primary care physicians regarding patients who drink too much.