Category Archives: Primary Care

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

 

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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 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.

 

VA Ambulatory Report 8.16.17 – Falls in the Elderly and Urinary Retention in Women

Thanks Beth for the awesome case of a 90 yo F with pmhx of HTN, CKD presenting after multiple falls who developed urinary retention and fecal incontinence found to have cervical spine myelopathy from spinal stenosis.

Key Learning Points

  • Approach to a patient with falls:  Consider a physiologic approach thinking about the systems that need to be functioning properly to walk: cognition, motor strength, sensation, musculoskeletal apparatus, cardiovascular fitness, navigable environment
  • Use the CHIP rule for determining which patients presenting to urgent care or the ambulatory setting need a head CT.  The Canadian head CT rule is for patients with loss of consciousness
  • The Timed Get-Up and Go test is helpful for assessing falls risk

 

Falls in the elderly

Step 1– Assess if the fall is consistent with syncope or pre-syncope vs. mechanical cause.

Step 2 – Assess the patient for injuries related to the fall.

  • When to get a head CT?
  • Decision rules to help us decide who needs a head CT after a fall.  The Canadian CT Head Rule is often applied in the Emergency setting and only applies to patients with loss of consciousness.  The Canadian head CT rules are the most widely validated.
  • For the ambulatory and urgent care setting you could consider using the CHIP rule because it applies to patients without loss of consciousness. Note that the CHIP rule recommends head CT in patients over 60 years of age.  This is a nice reminder that our older patients are at a much higher risk of subdural hematomas due to cerebral atrophy even with minor head trauma.

 

Step 3 – Evaluate for the etiology of the fall

Falls in the elderly are multifactorial and each fall could have a different etiology so needs to be evaluated separately.

You can use a physiologic approach to falls.  Think about all the systems you need to walk (which is actually a very complex task!):

  • Cognition
    • Dementia from any cause
    • Dementias associated with decreased physical functioning: parkinsons, spinal muscle atrophy
    • Normal pressure hydrocephalus
    • Drugs and toxins: alcohol, medications (see below)
  • Motor strength
    • Primary muscle disease
    • Stroke
    • Myelopathy
    • Neuromuscular junction disorder
  • Sensation
    • Peripheral neuropathy
    • Poor vision
    • Vestibular dysfunction
  • Musculoskeletal apparatus
    • Osteoporosis
    • Fracture
    • Ligamentous Injury
  • Cardiovascular fitness
    • Orthostatic hypotension
    • Arrythmias
  • Navigable environment
    • Lighting, irregular floor surfaces, unsafe stairs, cords and carpets
  • Medications (always include as a category of your differential in the elderly!)
    • Sedative-hypnotics, TCAs, antihypertensives, cardiac medications, corticosteroids, NSAIDs, anticholinergic meds, hypoglycemic agents

 

Timed Up and Go Test

  • Can be used to help with the global gait assessment
  • How to perform: Instruct the patient to get out of the chair (without using armrests), stand up, walk forward 10 feet, turn around and walk back to chair, sit down.
  • Normal is < 10 seconds and indicates the patient is mobile.  > 20 seconds indicates the patient is variably mobile.  > 30 seconds indicates impairments in mobility
  • Aside from timing, observing the patient’s ability to perform each maneuver of the test can help you determine what area the patient is deficient .

Interventions for abnormal results of the Timed Up and Go test (Table copied from Preventing Falls in the Geriatric Population reference below)

Observation Significance Intervention
Difficulty rising from chair Proximal muscle weakness PT referral for lower extremity strengthening
Staggering or reported dizziness upon rising Possible orthostasis Check orthostatic vital signs; review medications that may contribute to orthostasis
Pill-rolling tremor, stooped posture, shuffling/festinating gait Possible parkinsonism Consider neurology referral
Increased sway, magnetic gait Possible normal pressure hydrocephalus Ask about urinary incontinence and memory issues. If these are highly suspected, consider head CT
Path deviation Possible peripheral neuropathy, cerebrovascular disease Consider neuropathy workup, examination of feet, PT referral for assistive device
Slow, antalgic gait Pain from osteoarthritis, peripheral neuropathy, podiatric disorders Pain control, examination of feet

 

Differential for Urinary Retention in Women

  • Detrusor underactivity: aging, DM, neurologic disease (stroke, spinal cord compression),
  • Outflow obstruction: pelvic organ prolapse, pelvic masses
  • Functional: Dysfunctional voiding, Detrusor sphincter dyssynergia, bladder neck obstruction
  • Meds: Most common: anticholinergic and sympathomimetic
  • Infection – UTI, genital herpes

 

Smits M, et al. Predicting intracranial traumatic findings on computed tomography in patients with minor head injury: the CHIP prediction rule. Ann Intern Med. March 20, 2007;146(6):397–405.

AAFP article on falls in the elderly: http://www.aafp.org/afp/2000/0401/p2159.html

 

 

VA Ambulatory Report 8.2.17 – Weight loss and artificial valve endocarditis

Thanks Tim for presenting the case of a 76 yo M with a pmhx of AS s/p valve replacement presenting to clinic with subacute fatigue, fevers, and weight loss found to have endocarditis likely from one of the HACEK organisms with final culture results still pending.

Key Learning Points

  • If your baseline work-up (see details below) of weight loss in the elderly is normal, the likelihood of malignancy is very low.  There is no need for further testing, but you should continue with close follow-up.
  • TAVR is indicated for severe AS with symptoms and prohibitive surgical risk but also been shown to be non-inferior for high and intermediate surgical risk patients
  • Complications of artificial heart valves include: infection, thromboembolism, obstruction, regurgitation, and hemolytic anemia
  • HACEK organisms most often will grow in blood cultures but can take longer than our more common strep and staph species.

 

Weight loss in the elderly (flash back to report pearls from 6.7.17!)

  • Work-up is directed by history and physical but at a minimum should include: CBC, BMP, LFTs, TSH, CRP, ESR, LDH, UA, CXR, FOBT, maybe abdominal ultrasound
  • A prospective study demonstrated that if this baseline work-up is normal none of the patients went on to have malignancy demonstrated on additional testing. Therefore if the baseline work-up is normal, no further testing is necessary but continue with close follow-up.
  • AAFP Practice guidelines for Unexplained Weight Loss in Older Adults

 

Artifical Heart Valves

  • Types of artifical valves
    • When choosing between bioprosthesis vs. mechanical valves it should be a shared decision with the patient. Things to consider:
      • Longevity of the valve: Mechanical heart valves last 20-30 years vs. 10-15 years with bioprosthetic valves. Consider mechanical heart valves most often in patients < 60 years and bioprosthetic valves in patients > 70 years
      • Anticoagulation: Required in mechanical valves
    • Ball and cage valves: Phased out ~ 20 years ago, very durable but more complications including thromboembolism, migration of the whole valve, and the ball getting stuck in the cage
  • Methods for valve replacement: Surgical vs. TAVR
    • The PARTNER trial demonstrated non-inferiority of TAVR vs. SAVR for high surgical risk patients
    • Indications for TAVR:
      • Severe AS with symptoms and prohibitive risk for surgical replacement
      • Severe AS with symptoms and high surgical risk
        • Patients could also undergo SAVR
        • The PARTNER trial demonstrated non-inferiority of TAVR vs. SAVR for high surgical risk patients
      • TAVR is a reasonable alternative for patients at intermediate surgical risk depending on patient specific variables
        • PARTNER II trial demonstrated non-inferiority for TAVR vs. SAVR in intermediate risk patients
      • Contraindicated for bicuspid aortic valves
      • TAVR has not been studied in asymptomatic patients and therefore is not recommended.  Patients should be monitored clinically for development of symptoms.
  • Complications of artificial valves
    • Infection
    • Thrombus
      • Prosthetic valve thrombus leading to obstructive symptoms
      • Thromboembolism
    • Valve obstruction
      • Can be due to: leaflet fibrosis, Calcification, pannus formation, or thrombus
        • LT taught us about a patient he had with pannus formation which is fibrous tissue ingrowth around the valve.  This is much less common than other causes of obstruction
      • For dx: get echo to determine valve gradient and consider CT to better characterize the mass on the valve.  The patient may need surgery for diagnosis and treatment.
    • Valve regurgitation
      • Can occur both through the valve itself and paravalvular
      • Due to leaflet degeneration, calcification, endocarditis, thrombus, or pannus formation
    • Hemolytic Anemia

 

Endocarditis

  • HACEK organisms: Although historically classified as culture negative endocarditis, our current culture methods can grow these organisms but they take longer to grow (Median time is ~ 3 days).
  • Most common cause of culture negative endocarditis: fastidious organisms and strep species in patients already on antibiotics.
    • Diagnosing Q fever endocarditis
      • Phase I IgG antibody titer should be > 800
        • Duke’s criteria include microbiological evidence of infection. Major criteria: IgG Phase I titer > 6400. Minor criteria is a titer > 800
  • Shout out to Rabih’s prior morning report pearls on endocarditis breaking the differential down between culture positive and culture negative endocarditis.

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References:

PARTNER Trial: Smith, Craig R., et al. “Transcatheter versus surgical aortic-valve replacement in high-risk patients.” New England Journal of Medicine 364.23 (2011): 2187-2198. http://www.nejm.org/doi/full/10.1056/NEJMoa1103510#t=article

PARTNER II Trial: Leon, Martin B., et al. “Transcatheter or surgical aortic-valve replacement in intermediate-risk patients.” N Engl J Med 2016.374 (2016): 1609-1620.  http://www.nejm.org/doi/full/10.1056/NEJMoa1514616

AHA/ACC Guidelines for management of Valvular Heart Disease: http://circ.ahajournals.org/content/early/2017/03/14/CIR.0000000000000503

Ambulatory Report 7.26.17 – Charles Bonnet Syndrome, Alice-in-Wonderland syndrome, and high output heart failure!

Double Ambulatory Report Cases!
Case 1: LT presented a case of his primary care patient of 30 years!  The case was an elderly male pmhx of CAD, Afib, macular degeneration presenting with left visual field hallucinations found to have Charles Bonnet syndrome.
Case 2: Thanks Lily for presenting this interesting and yet to be solved case of a young male with a history of severe eczema on topical steroids, bloody bowel movements, who presents with subacute lower extremity edema and anemia.
Takeaways:
  1. Charles Bonnet syndrome: visual hallucinations that occur in people with vision loss due to disinhibition of the visual cortex
  2. Divide your differential for lower extremity edema into unilateral or bilateral causes.
  3. High output heart failure can be seen in many disease states including anemia, obesity, beriberi, and hyperthyroidism.
Charles Bonnet syndrome: 
  • Visual hallucinations in individuals with vision loss
  • Pathophysiology is theorized to be due to visual sensory deafferentation leading to disinhibition of the visual cortex which then fires spontaneously
  • Can occur in visual loss due to any cause including macular degeneration, optic nerve pathology, stroke, etc
  • The hallucinations can be non-formed (lines, flashes, shapes) or formed (people, scenes)
  • May be more common than we realize due to patients underreporting and clinicians mis-diagnosing as psychosis or dementia

 

Alice-in-Wonderland Syndrome
  • Episodes of visual hallucinations, bizarre perceptual distortions (usually body size distortion), or impairments in sense of time
  • Can be seen in migraines, temporal lobe epilepsy, brain tumors, psychoactive drugs,  or EBV infections
Differential diagnosis of lower extremity edema
  • Unilateral
    • Cellulitis
    • Clot
    • Lymphedema
    • Asymmetric venous stasis
  • Bilateral
    • Nephrotic Syndrome
    • Cirrhosis
    • Heart Failure
    • Low albumin state or protein loss
      • protein-losing enteropathy
      • Malnutrition
    • Refeeding syndrome
    • Pregnancy
    • Hypothyroidism
    • Venous stasis
    • Increased capillary permeability due to sepsis, burns, trauma, allergic reaction
    • Drugs: vasodilators, CCB, alpha-blockers, NSAIDs, steroids, androgens, estrogen, gabapentin, ropinirole, pramipexole, docetaxel, cisplatin
High Output Heart Failure
  • Hemodynamic characteristics: Elevated cardiac output, low SVR, increased oxygen consumption
  • Leads to neurohormonal activation —> reduced renal blood flow — > chronic volume overload due to retention of salt and water (See diagram below)
  • Patients will have symptoms of volume overload similar to low output heart failure
    • However, they will have warm extremities due to low SVR and vasodilatation
  • Causes:
    • Physiologic: excitement, anxiety, stress, exercise, pregnancy, fever
    • Pathologic
      • Obesity
      • AV shunts
      • Liver disease
      • Lung disease
      • Myeloproliferative disorders
      • Sepsis
      • Hyperthyroidism
      • Anemia
      • Beriberi
      • Dermatologic disorders (psoriasis)
      • Certain renal disorders (AV fistula)
      • Carcinoid syndrome
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Ambulatory Report 7.19.17 – Secondary Hypertension and a Hemorrhagic Stroke in a young patient

Thanks John for presenting this great case!  We discussed the case of a 31 yo male with a pmhx of hypertension and hemorrhagic stroke who was presenting for primary care now undergoing a work-up for secondary hypertension.

High-yield pearls

  • The most common causes of a hemorrhagic stroke in a young person are vascular malformations and hypertension
  • Consider an age-based approach to secondary hypertension work-up
  • LT pearl: If you are concerned about pheo, check orthostatics.  Untreated pheo patients will have positive orthostatics because they are chronically vasoconstricted and cannot adjust adequately to postural changes
  • Recognize lots of medications and dietary sodium will affect your renin/aldosterone ratio.  If your patient is on an ACEi or ARB, you do not need to stop the medication in your first pass you evaluation but know that a normal result does not exclude primary hyperaldosteronism.

 

Hemorrhagic CVA in the young:

  • Most frequent RISK FACTOR: tobacco use, HYPOcholesterolemia, HTN, alcohol use
  • Most frequent ETIOLOGY: vascular malformation and HTN
  • The final neurologic outcome was favorable in 60%
  • Causes overall:
    • Aneurysm/vascular malformation
    • Trauma
    • Severe HTN
    • Tumor
    • Septic/mycotic aneurysm
    • Bleeding d/o
    • CNS infection (eg HSV encephalitis)
    • Vasculitis
    • Drugs (cocaine, meth)
    • Secondary transformation from central venous thrombosis

 

Secondary Hypertension

Who should I work-up a patient for secondary hypertension?

  • 5-10% of all adults with HTN will have a secondary cause of HTN
  • Consider evaluation in patients with:
    • Resistant HTN: Defined as inadequately controlled BP when on three anti-hypertensives one of which must be a diuretic
    • Early or late onset HTN
    • Severe or accelerated course of HTN
    • Antihypertensive drug intolerance
    • Suggestive features on history or physical

When thinking about secondary hypertension consider an age-based approach to focus your differential. (Thanks for sharing Abbi and Jackie!)

afp20101215p1471-t3

Secondary Hypertension Differential and Suggestive Clues on history, physical, and basic labs

  • Renal Vascular Disease: Renal artery stenosis or fibromuscular dysplasia
    • Look for creatinine increases by >30% after starting ACEi or ARB, asymmetric size of kidneys, recurrent flash pulm edema, bruit on exam (not very sensitive)
  • Primary renal disease
    • Will see abnormal creatinine and UA
  • Endocrine causes
    • Pheochromocytoma
      • Triad; headache, palpitations, sweating,
      • LT pearl: check orthostatics!  Untreated pheo patients are chronically vasoconstricted so cannot adjust blood pressure with positional changes
    • Hyperaldosteronism
      • Unexplained hypokalemia, urine potassium wasting
      • One half of patients will have normal serum potassium
      • Typically mild HTN presenting in middle age
    • Cushing’s
      • Cushinoid features on physical exam
      • History of steroid use
    • Hypothyroid
    • Primary hyperparathyroidism
      • Hypercalcemia
  • Coarctation of the Aorta
    • Diminished or delayed femoral pulses
    • Asymetric BPs: BP in right arm > left arm or HTN in arms and low BP in legs
  • OSA
    • Obesity, daytime somnolence, snoring
  • Drugs
    • Cocaine, amphetamines
  • Medications
    • NSAIDs, OCPs, antidepressants, calcineurin inhibitors, decongestants, steroids,

 

Things that affect renin/aldo ratio: 

  • Meds
    • Mineralocorticoid receptor antagonist
    • Diuretics
    • ACEi or ARB
      • You do not need to take your patient off their ACEi or ARB in your first pass work-up because many with primary hyperaldosteronism will have an abnormal result.  However, if the result is normal you cannot exclude primary hyperaldosteronism and may need to recheck it off the medication.
    • Beta blockers
    • Clonidine
    • NSAIDs
    • SSRIs
    • OCPs
  • Hypokalemia/Hyperkalemia
  • Na restricted diet/Na loaded diet
  • Pregnancy
  • Renovascular HTN
  • Malignant HTN
  • Liddle syndrome: Liddle syndrome is a genetic disorder characterized by early, and frequently severe HTN with low plasma renin activity, metabolic alkalosis, hypokalemia, and normal to low aldosterone.

At the VA, endocrine clinic helps with obtaining this test and providing your patient with the appropriate instructions to avoid spurious results.

 

References:

Intracranial hemorrhage in Young People: http://stroke.ahajournals.org/content/30/3/537

Age Based Approach to Secondary Hypertension from the AAFP: http://www.aafp.org/afp/2010/1215/p1471.html