Adults

The risk of recurrent ischemic stroke can be reduced by managing modifiable risk factors and instituting a regimen of mechanism-specific secondary stroke prevention. Strategies for secondary prevention should be instituted as early as possible. Poststroke monitoring of risk metrics, lifestyle behaviors, and medication recommendations is of key importance.

Importance: Accurate assessment of intravascular volume facilitates management decisions about fluid management in patients with volume overload.

Objective: To identify the most accurate clinical examination, radiographic, and laboratory findings for assessing volume overload in nonintubated patients.

Data sources and study selection: MEDLINE was searched (1946 to January 6, 2026) to identify peer-reviewed English-language studies about the diagnostic accuracy of the clinical examination of spontaneously breathing patients with intravascular volume overload.

Data extraction and synthesis: Three authors independently extracted data for each finding and calculated sensitivity, specificity, and likelihood ratios (LRs). A 2-level mixed logistic regression model was used to pool estimates.

Results: Forty studies, involving 11 490 adult patients, were included, with a prevalence of volume overload of 35% to 69%. Thirty-three of those studies evaluated patients with dyspnea. Prevalence of volume overload was more likely when the physical examination revealed jugular venous distention with the highest point of pulsation more than 3 cm in a vertical line above the sternal angle (LR, 4.1 [95% CI, 2.9-5.6]; specificity, 92%), lower extremity edema (LR, 2.2 [95% CI, 1.5-3.1]; specificity, 80%), or crackles on auscultation (LR, 2.7 [95% CI, 1.7-4.5]; specificity, 81%). Vascular congestion on chest radiography increased the likelihood of intravascular volume overload (LR, 5.9 [95% CI, 2.9-12.0]; specificity, 91%). Point-of-care ultrasonography that identified bilateral pulmonary B-lines suggested volume overload (LR, 4.0 [95% CI, 2.6-6.1]; specificity, 77%), and absence of pulmonary B-lines made volume overload unlikely (LR, 0.09 [95% CI, 0.04-0.23]; sensitivity, 93%). Inferior vena cava collapsibility index of less than 50% increased the likelihood of volume overload (LR, 3.9 [95% CI, 2.5-6.1]; specificity, 79%), and a collapsibility index of at least 50% made it less likely (LR, 0.22 [95% CI, 0.11-0.45]; sensitivity, 82%). Point-of-care ultrasonographic measurement of jugular venous pressure (JVP; >8 cm) also increased the likelihood of volume overload (LR, 2.8 [95% CI, 2.2-3.5]; specificity, 71%), although JVP of 8 cm or less identified patients less likely to have volume overload (LR, 0.26 [95% CI, 0.20-0.33]; sensitivity, 81%). A plasma brain-type natriuretic peptide (BNP) level of 100 ng/mL or higher was the single best test to identify those most likely to have volume overload (LR, 6.9 [95% CI, 2.4-20.4]; specificity, 87%), and a normal value made it less likely (LR, 0.14 [95% CI, 0.08-0.24]; sensitivity, 87%).

Conclusions and relevance: A BNP level of 100 ng/mL or higher and presence of vascular congestion on chest radiography may be the most useful tests to identify patients with volume overload. Absence of pulmonary B-lines using point-of-care ultrasonography or BNP levels of less than 100 ng/mL may be most useful to exclude volume overload.

Calcium pyrophosphate deposition (CPPD) disease is caused by CPP crystal accumulation in musculoskeletal tissues, leading to inflammation
Symptomatic CPPD disease (formerly known as “pseudogout”) is more common in older than younger adults and typically affects joints with previous damage. Chondrocalcinosis visible on radiographs affects 10% of adults and 50% of those older than 80 years, but most people are asymptomatic and findings are noted incidentally.1

The most common presentation is acute inflammatory monoarthritis affecting the wrists or knees, which resolves within 4 weeks
Extra-articular structures can also be affected, leading to acute inflammatory tendinitis. Crowned dens syndrome comprises 5% of CPPD disease presentations and can mimic bacterial meningitis, manifesting with acute cervical neck pain, fever, and elevated inflammatory markers with CPPD at C1 to C2, seen on computed tomography. The chronic (> 3 mo) inflammatory phenotype presents with hand or wrist symmetric polyarthritis, or with recurrent flares, and can be misdiagnosed as seronegative rheumatoid arthritis. Calcium pyrophosphate deposition disease and osteoarthritis can co-exist — underlying CPPD disease should be considered in patients with osteoarthritis at atypical locations (e.g., metacarpophalangeal joints, wrists, ankles, shoulders, elbows).2

Diagnosis can be confirmed with CPP crystals identified from synovial fluid, or the presence of the crowned dens syndrome
Although used for research, the 2023 Classification Criteria have high sensitivity (99.2%) and specificity (92.5%), thereby providing a diagnostic framework.2 Supportive diagnostic features include acute knee or wrist inflammatory arthritis in an older adult, osteoarthritis at atypical areas, or CPPD on imaging.3

Patients younger than 60 years at diagnosis should be assessed for associated metabolic diseases
Investigations for secondary causes of CPPD disease include calcium (hypercalcemia), parathyroid hormone (hyperparathyroidism), ferritin, transferrin saturation (hemochromatosis), magnesium (hypomagnesemia), and alkaline phosphatase (hypophosphatasia).2

Corticosteroids, colchicine, and nonsteroidal antiinflammatory drugs can treat acute flares4
Inflammatory arthritis lasting more than 3 months or recurrent flares (> 2/yr) should prompt rheumatology referral for consideration of chronic suppressive colchicine, hydroxychloroquine, or methotrexate (Appendix 1, available at www.cmaj.ca/lookup/doi/10.1503/cmaj.250933/tab-related-content).5

Approximately 1 in 7 individuals are affected by perinatal depression, defined as a depressive episode occurring during pregnancy or within 12 months after delivery. Although the diagnostic criteria are similar to those of major depressive disorder, perinatal depression may also include symptoms such as difficulty forming an emotional attachment with the fetus or infant, persistent doubts about parenting abilities, and intrusive thoughts of harm to self or infant.1 Mental health conditions are leading contributors to maternal mortality in the US; among reporting states, the rate of death from perinatal suicide ranges from 4.2 to 21.4 per 100 000 pregnancies.2 Untreated or undertreated perinatal depression increases other maternal risks, including limited engagement in care, impaired relationships, substance use, preeclampsia, and suicide, as well as fetal or neonatal risks, including preterm birth, low birth weight, and disrupted attachment with long-term developmental consequences.3 Individuals from marginalized communities, such as those who are non–English speaking, uninsured, or geographically isolated, experience a higher prevalence of perinatal depression and are at increased risk of underdiagnosis and undertreatment.3

Risk factors for perinatal depression include a personal or family history of depression, abuse, stressful life events, low socioeconomic status, adolescent or single parenthood, and pregnancy complications, such as preterm birth or pregnancy loss. Each factor individually confers only a small increase in risk, making accurate prediction based on clinical factors challenging.4 Therefore, to facilitate early identification and treatment, universal screening during and after pregnancy is recommended. The American College of Obstetricians and Gynecologists (ACOG) recently issued 2 Clinical Practice Guidelines on perinatal mental health, 1 on screening and diagnosis5 and 1 on treatment and management,3 highlighting opportunities for obstetricians to address existing health gaps.