10/19 Presby report: geriatrics pearls

Thanks to Lindsey Haddock for an awesome and very informative SAR report on new literature in geriatrics! We discussed several important recent trials focused on older populations:

#1

  • The “After Eighty” study: how do we treat people >80 with NSTEMI or UA?
    • this study looked at invasive intervention (PCI or CABG) vs optimum medical management in an older population with a composite endpoint: death, MI, stroke, revascularization
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The hazard ratio of invasive vs conservative management crosses 1 around age 90, implying that the benefit of invasive intervention fades continuously between age 80-90. The NNT for invasive intervention was 4.8. Tegn et al, Lancet 2016.

Take away: invasive intervention for UA or NSTEMI may benefit patients >80, but there may be diminishing benefit as they get older. Remember to consider other comorbidities (dementia, cancer, advanced COPD, etc) that may diminish the benefit they get from an invasive intervention!


#2

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This study was a subgroup analysis of patients >75 who were part of the SPRINT trial.

  • Again, they analyzed the two groups: intervention (goal SBP <120) and conservative (goal SBP <140) within the older subgroup. They also collected data on frailty and gait speed.
  • Findings: over 3 years, intensive BP control reduced incident CV disease by 33% and mortality by 32%, with NNT = 27 to prevent one negative CV event

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Stratified by frailty, both ‘frail’ and ‘fit’ patients seemed to benefit from intensive BP control. JAMA 2016.

The major caveat to this analysis (and to SPRINT): it excludes patients with stroke, DM, HFrEF, dementia, recent unintentional weight loss, expected survival of ❤ years, or who were nursing home residents; this obviously excludes a big proportion of the patients we see!

Take away: if an older patient is tolerating a lower blood pressure, you don’t necessarily need to de-escalate; if they have a BP >120 and don’t have other major reasons not to do add on an additional agent (falls, polypharmacy, life expectancy etc), you can consider it as it may be beneficial.


#3

Screen Shot 2017-10-19 at 2.18.42 PM.pngThis meta-analysis suggested that in-hospital use of anti-psychotics did NOT result in improvements in:

  • short-term mortality
  • duration or severity of delirium
  • hospital or ICU length of stay

It’s important to note that many of those studies were heterogenous in terms of included patient populations, and that other studies have shown conflicting results. Many of the trials also did not evaluate for symptomatic relief, which is one of the main reasons we use antipsychotics like Haldol in the hospital

Dr. Uy pointed out that one of the reasons antipsychotics may not be as beneficial as we think is that we may just trade acute hyperactive delirium for a longer period of delirium with a longer ‘tail’, or may push them into hypoactive delirium which continues at home after discharge.

References

  1. Tegn et al. After Eighty Study. Lancet 2016.
  2. Williamson et al. Intensive vs Standard Blood Pressure Control and Cardiovascular Disease Outcomes in Adults Aged ≥75 Years. JAMA 2016.
  3. Neufeld K et al. Antipsychotics for Prevention and Treatment of Delirium in Hospitalized Adults: A Systematic Review and Meta-analysis. J Am Geritr Soc 2016.

 

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10/18 Presby report: inflammatory back pain

 

Thanks to Dr. Lan Chen for going through her approach to lower back pain and dropping some awesome rheum pearls!

Your physical exam provides important clues to the diagnosis of AS, its extra-articular manifestations, as well as other rheumatologic conditions

  • FABER/Patrick’s test: can suggest sacroiliitis
  • Lumbar spine exam (although SI inflammation/pain is more common than L-spine pain)
  • Nails: can show pitting suggestive of psoriatic arthritis
  • Skin: psoriatic plaques, erythema nodosum, pyoderma gangrenosum, keratoderma blenorrhagicum (reactive arthritis)
  • Eyes: uveitis
  • Tongue erosions (suggestive of reactive arthritis)

Recall some key features of inflammatory back pain:

  1. Onset of back discomfort before the age of 40 years;
  2. Insidious onset lasting more than 3 months;
  3. Improvement with exercise; No improvement with rest.
  4. Pain at rest or at night
  5. Profound morning stiffness

Presence of four out of five of those features has ~70% sensitivity and specificity for ankylosing spondylitis.

Imaging

Dedicated imaging of the sacroiliac joint is perhaps more useful than general spine or L-spine imaging, since sacroiliitis is more common than L-spine inflammation.

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CT scan: normal SI joint. Note the clean, linear joint space

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CT scan: sacroiliitis. Note the shaggy, narrowed joint space 

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MRI showing marrow edema adjacent to the joint space in a patient with sacroiliitis

In early disease (first few years of symptoms), only MRI is likely to be sensitive enough to pick up SI joint changes; as the disease progresses, CT becomes more sensitive (~5 years into disease course). X-rays are really only useful in advanced disease.

Treatment

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Zochling J, et al. Ann Rheum Dis 2006.

Additionally:

  • Ustekinumab and secukinumab are anti-IL23/IL17 biologics that can be used to treat AS
  • Apremilast is a PDE4 inhibitor that can also be used for AS

There are multiple causes of inflammatory back pain:

  • Primary ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • Enteropathic arthritis
    • Crohn’s disease
    • Ulcerative colitis
  • Juvenile ankylosing spondylitis
  • Undifferentiated spondyloarthropathies

Other rheum pearls

  • Obesity may be a risk factor for autoimmune disease
  • Gonococcal arthritis tends to more commonly affect upper extremity joints, while reactive arthritis tends to affect lower extremity joints

References

 

10/16 Presby report: MSK complications of diabetes, diabetic myonecrosis

Thanks to Samantha Parker for presenting the case of a young female type 1 diabetic who presented with bilateral thigh pain and was found to have diabetic muscle necrosis (aka myocnecrosis).

We discussed several of the MSK complications that poorly controlled diabetics are susceptible to; many of these complications are due to diabetic microvascular disease.

Approach to MSK pain in poorly controlled diabetics

  • Hand
    • Carpal tunnel
    • Dupuytren’s contracture
    • Flexor tenosynovitis
    • Diabetic sclerodactyly
    • Limited joint mobility
  • Shoulder
    • Adhesive capsulitis
    • Calcific periarthritis
    • Limited joint mobility
  • Lower limb
    • Neuropathic arthropathy (Charcot joint: foot and ankle)
    • Diabetic muscle infarction/myonecrosis (thigh and calf)
    • Osteonecrosis (knee)
    • Osteoarthritis (knee)
  • Spine
    • Diffuse idiopathic skeletal hyperostosis (DISH)

Diabetic myonecrosis

  • occurs most commonly in the thigh or calf
  • often no history of trauma, and in ~10% of cases can be bilateral
  • typically develops after 10-15 years of poorly controlled diabetes
  • CK may be moderately elevated (usually <1000), and MRI may show evidence of muscle damage and edema
  • Treatment: low dose ASA or NSAIDs, rest/analgesics, possible role for surgical excision
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R thigh muscle infarction. Radiopedia.

Other pearls

  • Use of warfarin and corticosteroids may predispose to calciphylaxis
  • Pyomyositis can present similarly to diabetic myonecrosis, and depending on the location of the infected muscle, can present with proximal lower extremity drainage (ex: psoas pyomyositis)
  • Complex regional pain syndrome: usually affects distal limbs characterized by pain, swelling, limited ROM, vasomotor instability, skin changes, and patchy bone demineralization; usually triggered by trauma or surgery

References

Cagliero E, Apruzzese W, Perlmutter GS, Nathan DM. Musculoskeletal disorders of the hand and shoulder in patients with diabetes mellitus. Am J Med 2002; 112:487.

Kapur S, Brunet JA, McKendry RJ.Diabetic muscle infarction: case report and review. The Journal of Rheumatology January 2004, 31 (1) 190-194

 

10/11 Presby report: PD peritonitis

We discussed an elderly woman with ESRD who presented with progressive abdominal pain, distention and fevers and was diagnosed with PD (peritoneal dialysis-associated) peritonitis, which was ultimately found to be due to TB!

What is peritoneal dialysis?

In the simplest terms, PD involves the instillation of dialysis fluid into the peritoneum with the goal of achieving solute clearance and ultrafiltration across the peritoneal membrane.

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Dialysis fluid ‘dwells’ in the peritoneum while solute and volume move into it; it is then removed via the peritoneal catheter at the end of the dwell

There are three specific infectious complications of PD catheters: 1) PD peritonitis, 2) tunnel infection and 3) exit site infection

The microbiology of PD peritonitis differs somewhat from spontaneous bacterial peritonitis (SBP).

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Microbiology of PD peritonitis. Glickman 2017

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  • NB: unlike SBP, where >250 PMNs or a +culture is necessary for the diagnosis, about 10% of patients with PD peritonitis present without >100 WBCs, so it’s important to have a high suspicion for it
  • It’s often a difficult decision as to whether to try to preserve the catheter or to pull it. In general, fungal, mycobacterial and pseudomonal peritonitis necessitate catheter removal.
  • You can try to treat through other forms of bacterial PD peritonitis, unless it’s a recurrent or refractory infection
  • Recurrent episodes of peritonitis can make the abdomen less hospitable to PD, and can even lead to the development of peritoneal sclerosis, which may lead to small/large bowel obstruction, constipation, malnutrition and death

This patient ultimately had her peritoneal fluid tested for adenosine deaminase (ADA) given the concern for TB. A few quick notes:

  • It can be used to distinguish between tuberculous and malignant causes of lymphocytic pleural effusions/ascites, etc.
  • Test characteristics vary somewhat between different body sites, but for tuberculous ascites, ADA (particularly values >35) has a ~95% sensitivity and 96% specificity, a positive likelihood ratio of ~16 and a NLR of 0.09!

References

  1. Diagnostic accuracy of adenosine deaminase for tuberculous peritonitis: a meta-analysis. Arch Med Sci 2013.

  2. Akoh JA. Peritoneal dialysis associated infections: An update on diagnosis and management. World J Nephrol 2012.

10/10 HUP Report – Small Bowel Mass

Today we discussed an interesting case of a patient with longstanding Crohn’s disease, well-managed off immunosuppression, who presented with an enterovesicular fistula. This is actually a really RARE complication of Crohn’s disease (approximately 3%), and almost always requires surgical intervention. Aside from being secondary to active inflammation from his IBD, this new clinical finding could be secondary to a small bowel neoplasm (small bowel cancer is also really rare, but the rate is increased in Crohn’s disease patients).

Here is our basic differential for a small bowel mass:

Malignant

  • Neuroendocrine tumor
  • Adenocarcinoma
  • Sarcoma
  • Lymphoma
  • Metastatic disease (hematogenous spread or direct spread from peritoneal carcinomatosis)

Benign

  • Lipoma
  • Fibroma
  • Leiomyoma
  • Adenoma
  • Desmoid tumor

Infectious

  • Tuberculosis
  • Abscess
  • Histoplasma

This patient’s biopsy was consistent with neuroendocrine tumor, and he had numerous metastases — this is a common finding at the time of diagnosis due to indolent and asymptomatic growth in many patients. First line treatment for neuroendocrine tumors is usually somatostatin receptor analogues. Symptomatic surgical debulking or curative surgical resection can be considered in appropriate candidates, but is less common. Prominent symptomatic liver mets can be managed with ablation techniques. Systemic chemotherapy can be attempted for refractory disease — everolimus, bevacizumab, and sunitinib have been used.

 

 

10/9 Presby report: hypertensive emergency, CSF xanthochromia, PRES

Thanks to Katie Flack for presenting a middle aged woman who woke up with a thunderclap headache and altered mental status, and was found to have hypertensive emergency. We talked about a lot of cool stuff and I tried to include most of it below!

Hypertensive emergency: classically defined as >180 systolic or >110 diastolic, or an acute rise in BP over a previously normal baseline; remember a person with lower baseline BPs can have hypertensive emergency at lower BPs!

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Varon et al 2003

Initial evaluation

  • CBC + smear (to rule out MAHA)
  • BMP (AKI)
  • Troponins (myocardial injury)
  • EKG (r/o ACS)
  • CXR (widened mediastinum, pulmonary edema)
  • Urinalysis (hematuria, proteinuria)
  • Head imaging (intracranial hemorrhage)

Management

Most patients with hypertensive emergency are chronically hypertensive, and have a rightward shift of their vascular autoregulation curves:

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Varon et al 2003

This is why reducing the BP too rapidly can have lethal consequences. Important: only patients with hypertensive emergency should have their BP lowered rapidly (generally ~10% in the first hour, total ~25% in the first 24h).

EXCEPTIONS TO THAT RULE

  • Acute phase of ischemic stroke: keep BP <185/110 in pts who are candidate for tPA and <220/120 in those that are not
  • Aortic dissection: rapidly (within 10-20 min) lower SBP to 100-120

 

Briefly, agents that can be used (in the ICU) for hypertensive emergency:

  • Esmolol
  • Labetalol
  • Nicardipine
  • Nitroglycerine
  • Nitroprusside
  • Oral agents (hydralazine, nifedipine, etc)

Other pearls

  • The sensitivity of CT head for SAH declines with time: nearly 100% within 6-12h of the bleed, but it decreases to ~60% by day 5
  • In patients with a high suspicion of SAH, consider an LP even if the HCT is negative to look for RBCs or xanthrochromia in the CSF (AHA stroke guidelines, class 1B)
    • Xanthochromia can be detected 2-4h after the SAH, and is present in 90% of SAH patients within 12 hours!
  • We talked briefly about PRES: posterior reversible encephalopathy syndrome
    • Mechanism unclear, but ?related to cerebral autoregulatory dysfunction
    • Most commonly linke to hypertensive emergency or the use of immunosuppressive drugs (tacrolimus, cyclosporine > sirolimus, bevacizumab)

References

  1. Varon J and Marik PE. Clinical review: The Management of Hypertensive Crises. Crit Care 2003.
  2. VBGs vs ABGs: https://lifeinthefastlane.com/ccc/vbg-versus-abg/

10/9 HUP Report – IgA Nephropathy

Today we discussed a case of acute kidney injury and proteinuria in a patient with well-controlled HIV, who was ultimately diagnosed with IgA nephropathy. It is important to remember that patients with well-controlled HIV have pretty much the same differential for glomerular disease as the general population.

In general, we classify glomerular diseases based on whether all glomeruli (diffuse) or only some (focal) are involved, and within each individual glomerulus whether the entire unit (global) or only part (segmental) is effected.

There are two broad syndromes of glomerular disease: nephrotic syndrome (which is characterized primarily by proteinuria >3.5 g/day) and nephritic syndrome (glomerular inflammation). Urinalysis findings of erythrocyte casts or dysmorphic red cells have a high specificity for glomerular pathology, which can also be suggested by hematuria and proteinuria.

Nephrotic Syndrome

Nephrotic syndrome can be a primary glomerular pathology, or it can be secondary to a systemic disease process (infectious, malignant, or medication-induced). Here is a basic differential for nephrotic syndrome:

  • Minimal change disease
  • Focal segmental glomerular sclerosis
  • Membranous glomerulopathy
  • Diabetic nephropathy

Nephritic Syndrome

Nephritic syndrome can be conceptualized based on mechanism of disease into three categories – pauci-immune (minimal immune cell infiltration), immune complex deposition, and anti-glomerular basement membrane antibody-mediated.

Pauci immune: seen in vasculitis (MPA, GPA, eGPA)

Anti-GBM antibodies: can have pulmonary manifestations (Goodpasture’s syndrome). Inherited collagen IV disorders can also effect renal function.

Immune complex deposition

  • IgA nephropathy
  • SLE nephritis
  • Infection-related glomerulonephritis
  • Membranoproliferative glomerulonephritis

In our patient, renal biopsy made the diagnosis of IgA nephropathy!