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

 


Filed under: Ambulatory, Cardiovascular Medicine, Morning Report, Primary Care Tagged: Ambulatory

Moffitt Pearls 7.19.17 – Morning Report – H&N infxn and more!

Image & Mini-case Potpourri!!!

Thank you Mike Thomashow for presenting a mini-case of an older patient with MM on chemotherapy with Ludwig’s Angina.

Thank you, HH for sharing the story of a young, otherwise healthy man admitted to the medical service who developed a sore throat and then several days later developed high fevers and rigors. Blood cultures returned positive fusiform bacteremia!

And finally, thank you to Brad Monash for telling us about space occupying lesions of infectious, malignant and inflammatory etiologies. Brad shared with us an image of a patient with Rosei Dorfman disease!

Key Pearls

  • Ludwig angina: infection begins in the floor of the mouth, is aggressive with rapid spreading cellulitis involving the submandibular space
  • Lemierre Syndrome is jugular vein suppurative thrombophlebitis: infection involvement of the carotid sheath vessels with bacteremia.
  • Airway stridor is the end game of airway compromise and requires emergent evaluation by ENT. Patient with airway concern need admission to ICU.
  • Space occupying lesions – 1) infections 2) malignant 3) inflammatory and NEW 4) infiltrative – including histiocytosis. Check out this great Clinical Care Conundrum – you may recognize several of the authors 🙂

 

 


Ludwig angina

  • Has been traditionally loosely applied to a heterogeneous array of infections involving the sublingual and submylohyoid (submaxillary) spaces.
  • True definition: infection begins in the floor of the mouth. An aggressive, rapidly spreading “woody” or brawny cellulitis involving the submandibular space.
  • Present without lymphatic involvement and generally without abscess formation.
  • Both the submylohyoid and sublingual spaces are involved.
  • The infection is often bilateral.

Microbiology of Ludwig Angina

  • Most common organism isolated from deep neck space infections is Streptococcus viridans. Most abscesses originating from the teeth also harbor oral anaerobes, including Peptostreptococcus species, Fusobacterium nucleatum, pigmented Bacteroides (eg, Prevotella melaninogenica [formerly Bacteroides melaninogenicus] and Porphyromonas spp), and Actinomyces species.
  • In immunocompromised patients, gram-negative aerobes may also be present.

Lemierre Syndrome

  • Jugular vein suppurative thrombophlebitis: infection involvement of the carotid sheath vessels with bacteremia.
  • Often preceded by pharyngitis, usually in association with tonsil or peritonsillar involvement. Other antecedent conditions include primary dental infection or infectious mononucleosis.
  • Infection progresses from the oropharynx to the parapharyngeal or lateral pharyngeal space. The anterior part of this space consists of the anterior neck muscles; the posterior section contains the carotid sheath that encloses the internal jugular vein, internal carotid artery, the vagal nerve, and lymph nodes

Head and Neck Infection – Overview of Microbiology

  • Epiglottitis à H. Flu
  • Peritonsil abscess à Group A Strep
  • Ludwigs angina (above)à tongue displacement (mixed peri-dontal including bacteroidies, Fusibacterium)
  • Actinomyces
  • Nocardia

Acute bacterial sialadenitis

  • Acute bacterial sialadenitis (suppurative sialadenitis) in the absence of sialolithiasis is a condition that typically affects older adults, malnourished, or postoperative patients. The parotid gland is most commonly involved. It is characterized by sudden onset of a very firm and tender swelling over the involved gland. Fever and chills are usually present, generally with fairly marked systemic toxicity. Purulent drainage can often be expressed from the effected duct orifice.
  • Staphylococcus aureus is the most frequent microbiologic isolate, but Streptococcus pneumoniaStreptococcus viridansHaemophilus influenzae, and Bacteroides species have also been isolated. Broad-spectrum therapy should be initiated. Prompt surgical drainage and decompression is required if an abscess develops.

Quick Guide based on patient characteristics:

  • ICU patient who is critical ill –> think Gram negative bacteria
  • Outpatient setting –> Staph aureus (Sjogrens is a risk factor)
  • More often in the pediatric or global population –> Mumps

 

Evernote: https://www.evernote.com/shard/s462/sh/4fa562e7-815d-41c9-a7a0-0b6cc002850b/6e5606181240beedc3afa93611cc6d9a


Filed under: Morning Report

ZSFG AM Report Pearls 7/18/2017: Syncope, Bradycardia, and Controversies in Risk Stratification!

Thank you to Mike Incze for presenting a case of symptomatic bradycardia with syncope from complete heart block that was initially thought to be due to hyperkalemia but has now persisted despite correction of electrolyte abnormalities.

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Top Pearls:

  • SF Syncope Rule is a controversial tool used to risk stratify patients presenting to ED with unexplained syncope using Hx of CHF, Hct <30%, Abnml EKG, SOB, SBP <90
  • Bradycardia DDx is broad but should include medications, electrolytes, ischemia, infiltrative and infectious etiologies.
  • A complaint of bradycardia should be evaluated initially by determining if stable or unstable (CP, SOB, AMS, low BP, evidence of end organ damage)

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SF Syncope Rule:

  • For patients with unexplained syncope
  • Potentially can be used to risk stratify and identify patients who need admission
  • NOTE: Controversial in the literature (with an impressive back and forth that is played out in Annals of Emergency Medicine)
    • Hx of CHF
    • Hct <30%
    • Abnormal EKG (Any non-sinus rhythm, ANY new change on EKG)
    • Shortness of Breath
    • Systolic BP <90mmHg at triage

If all absent, may be low risk for having a significant event in the next 30 days and may not need inpatient admission.

Note: Remember, at UCSF, ED providers decide about the need for admission and especially given the controversy about this “rule,” we would not recommend using this to frame your thoughts about the appropriateness of admissions.

Original Study:

  • Excluded pts w/ trauma, EtOH, or drug-associated loss of consciousness
  • Outcome measurement = serious outcome within 30 days of their ED visit (death, MI, arrhythmia, PE, stroke, subarachnoid hemorrhage, enami, procedural intervention, hospitalization, return ED visity)
  • The rule was 98% sensitive (95% confidence interval [CI] 89% to 100%) and 56% specific (95% CI 52% to 60%) to predict these events. In this cohort, the San Francisco Syncope Rule classified 52% of the patients as high risk, potentially decreasing overall admissions by 7%. If the rule had been applied only to the 453 patients admitted, it might have decreased admissions by 24%.

External Validation Study:

  • Sixteen of 61 (26%; 95% confidence interval [CI] 16% to 39%) patients with a serious outcome were not identified as high risk by the rule. Rule performance to predict serious outcomes was sensitivity 74% (95% CI 61% to 84%), specificity 57% (95% CI 53% to 61%); negative likelihood ratio 0.5 (95% CI 0.3 to 0.7) and positive likelihood ratio 1.7 (95% CI 1.4 to 2.0)

Response to External Validation Study:

  • Authors argue that the institution doing validation had small number of ED visits for syncope and a high number of admissions  for syncope
  • Also argue that they incorrectly applied the EKG part of the SF Syncope Rule in the validation study

 

Bradycardia:

Etiologies:

  • Medications: BB, CCB, Amio, Lithium, Digoxin, Clonidine, acetylcholinesterase inhibitors
  • Ischemia: Acute MI (15-25% of patients with acute MI)
  • Increased Vagal Tone: athletes, sleep, IMI
  • Metabolic: hypoxia, sepsis, myxedema, hypothermia, hypoglycemia, hyperkalemia
  • OSA
  • Increased intracranial cranial pressure (Cushing)
  • Infectious: Chagas, Lyme disease, legionella, Q fever, babesia, malaria, RMSF, lepto, yellow fever, dengue, trichinosis
  • Infiltrative/Myocarditis: sarcoid, amyloid, hemochromatosis
  • Treatment: none if asymptomatic, atropine, B1 agonists, or temp pacing

Sick Sinus Syndrome:

  • Features can include unprovoked sinus bradycardia, SA arrest, paroxysms of SB and atrial tachyarrhythmias, chronotropic incompetence w. ETT
  • Treatment: meds alone usually fail (Adequate tachy -> unacceptable brady) usually need combination of meds (BB, CCB, dig) for tachy & PPM for brady.

 

Sources:

  • Quinn J, McDermott D, Stiell I, Kohn M, & Wells G. (2006). Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 47(5): 448-454.
  • Birnbaum A, Esses D, Bijur P, Wollowitz A, Gallagher EJ. (2008). Failure to validate the San Francisco Syncope Rule in an independent emergency population. Ann Emerg Med. 53(2): 151-159.
  • Mendu ML, McAvay G, Lampert R, Stoehr J, Tinetti ME. (2009). Yield of diagnostic test in evaluating syncopal episodes in older patients. Arch Intern Med. 169(14): 1299-1305.

 

Also, a reminder about EKG Change in Hyperkalemia, check out prior Chief’s Blog Post:  https://ucsfmed.wordpress.com/2017/06/27/zsfg-am-report-pearls-6272017-non-stemi-st-segment-elevations-and-ekg-changes-in-hyperkalemia/

 

Evernote links

 


Filed under: Morning Report