My elderly patient is scheduled to undergo elective surgery? Is there an objective “stress test for the brain” that may predict postoperative delirium?

Possibly, in the near future! Although the pathophysiology of postoperative delirium (POD) is not fully understood, a recently proposed conceptual model of delirium may provide a basis for preoperative neurophysiologic testing1.

According to this model, delirium is a “consequence of the breakdown in brain network dynamics” precipitated by insults or stressors (eg, surgery) in persons with low brain resilience ie, low connectivity between brain regions and/or deficient neuroplasticity (the ability of brain to reorganize itself by forming new neural connections).  

As expected,  patients with strong baseline connectivity and optimal neuroplasticity would not be expected to have POD, whereas those with weakened connectivity (eg baseline cognitive dysfunction) and/or suboptimal neuroplasticity (eg due to aging) may be at higher risk. Transcranial magnetic stimulation (TMS)  is considered a powerful tool that measures the connectivity and plasticity of the brain through induced perturbation.  When applied in repetitive trains, TMS produces changes in cortical excitability that can be measured using electromyography and EEG,  and is thought to have the ability to assess neuroplasticity 2. If proven effective in predicting POD, it could revolutionize preoperative risk assessment in the elderly! Stay tuned!

 

Reference

  1. Shafi MM, Santarnecchi E, Fong TG, et al. Advancing the neurophysiological understanding of delirium. J Am Geriatr Soc 2017. DOI:10.1111/jgs.14748.
  2. Pascual-Leone A, Freitas C, Oberman L, et al. Characterizing brain cortical plasticity and network dynamics across the age-span in health and disease with TMS-EEG and TMS-fMRI. Brain Topogr 2011, 24:302-15.
My elderly patient is scheduled to undergo elective surgery? Is there an objective “stress test for the brain” that may predict postoperative delirium?

When should I suspect spinal epidural abscess in my 55 year old patient with severe back pain?

Up to 75% of patients with spinal epidural abscess (SEA) are misdiagnosed on their initial healthcare encounter1 , in large part related to the non-specific nature of back pain.  Potential “red flags” for infectious causes of low back pain include age >50 y, night pain, unremitting pain even when supine, duration > 6 weeks, fever, chills, night sweats, weight loss, conditions associated with Staphylococcus aureus bacteremia (eg intravenous drug use), incontinence, saddle anesthesia, and severe or rapidly progressive neurologic deficits1,2.   It cannot be overemphasized that up 50% of patients with SEA have no known risk factors,  one-half may have no fever and 20-40% lack leukocytosis1.

ESR and C-reactive protein (CRP) are almost uniformly elevated in SEA1 and can serve as a good starting point in excluding this condition.   In patients ≥50 y of age with low back pain, obtaining ESR routinely was suggested in 2002 for detection of systemic disease (eg cancer, infection)3.  Similarly, in a recent algorithm of severe back pain, routine measurements of ESR and CRP even in the absence of any neurological findings, has been recommended1.  Elevation of either ESR or CRP should raise suspicion for SEA and  lead to the consideration of MRI as clinically indicated.

References:

  1. Bond, A, Manian FA. Spinal epidural abscess: a review with special emphasis on earlier diagnosis. BioMed Res International 2016; http://dx.doi.org/10.1155/2016/1614328
  2. Della-Giustina. Acute low back pain: recognizing the “red flags” in the workup. Consultant 2013;53:436-440.
  3. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002;137:586-597.

 

Disclosure: The author of this post (FAM) also coauthored reference 1.

When should I suspect spinal epidural abscess in my 55 year old patient with severe back pain?

How exactly do urinary tract infections (UTIs) cause delirium in my elderly patients?

 UTIs are often considered in the differential diagnosis of causes of delirium in the elderly. Though largely speculative, 2 possible pathophysiologic basis for this association are suggested: 1. Direct brain insult (eg, in the setting of sepsis/hypotension); and 2. Indirect aberrant stress response, involving the hypothalamic-pituitary-adrenal [HPA] axis, sympathetic nervous system (SNS) and/or inflammatory pathways1-3.

One or both pathways can interact with the neurotransmitter and intracellular signal transduction systems underlying delirium in the brain, which may already be impaired in the elderly due to age-related or other pathologic changes. The indirect aberrant stress pathway suggests that not only can UTI-associated circulating cytokines cause delirium but pain and discomfort (eg, from dysuria) may also contribute via the HPA axis and SNS. If true, this explanation makes it unlikely for bacteriuria or pyuria to be associated with delirium in the absence of significant systemic inflammatory response or pain and discomfort.

 

References

1.Trzepacz P, van der Mast R. The neuropathophysiology of delirium. In Lindesay J,  Rockwood K, Macdonald A (Eds.). Delirium in old age, pp. 51–90. Oxford University Press, Oxford , 2002.

2.Flacker JM, Lipsitz LA. Neural mechanisms of delirium: current hypotheses and evolving concepts. J Gerontol A Biol Sci Med Sci. 1999; 54: B239–B246

3. Maclullich AM, Ferguson KJ, Miller T, de Rooij SE, Cunningham C. Unravelling the pathophysiology of delirium: a focus on the role of aberrant stress responses. J Psychosom Res. 2008;65:229–38.

Contributed by Henrietta Afari MD, Mass General Hospital, Boston, MA

How exactly do urinary tract infections (UTIs) cause delirium in my elderly patients?

Should I routinely consider the possibility of pulmonary embolism (PE) in my patients hospitalized for syncope?

Syncope is a well-known initial manifestation of pulmonary embolism (PE)1.  However, given the varied causes of syncope, determining the prevalence of PE among patients hospitalized for syncope is important.   

A recent NEJM study furthers our understanding of PE and syncope2.  This multicenter prospective study enrolled 560 patients not already on anticoagulation who were hospitalized for a first episode syncope.  Of 230 patients who had either a high pretest probability for PE, positive D-dimer assay or both, PE was diagnosed in 97 (17%, or nearly 1 of 6 of enrolled patients) based on CT or ventilation/perfusion scan. PE was found more frequently among patients with syncope of undetermined cause than those with an alternative explanation (25.4% vs 12.7%). 

The results of this study should make us consider, perhaps more frequently, the possibility of PE in patients hospitalized for first episode syncope not on anticoagulants, particularly those without an alternative explanation.

 

References 

  1. Thames MD, Alpert JS, Dalen JE. Syncope in patients with pulmonary embolism. J Am Med Assoc 1977;238:2509-2511. 
  2. Prandoni P, Lensing AWA, Prins MH, et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med 2016;375:1524-31.

 

Contributed by Rebecca Berger  MD, Department of Medicine, Mass General Hospital, Boston, MA.

Should I routinely consider the possibility of pulmonary embolism (PE) in my patients hospitalized for syncope?