EUHM Report: What is the etiology of Streptococcus anginosus?

The S anginosus group, often referred to as Streptococcus milleri , are commensals of the oropharyngeal, GI, and genitourinary microflora that can cause invasive  pyogenic infections in various sites. While more commonly associated with CNS, abdominal, head and neck, bloodstream, and thoracic infections, the three species that make up S anginosus have been associated with differing clinical manifestations.

Sunwoo, Bernie Y, and Wallace T Miller. “Streptococcus Anginosus Infections: Crossing Tissue Planes.” Chest. 146, no. 4 (2014): E121-125.

While more commonly associated with CNS, abdominal, head and neck, bloodstream, and thoracic infections, the three species that make up S anginosus have been associated with differing clinical manifestation.  The S anginosus group of organisms is known to be highly virulent and rapidly progressive, and it is not surprising that they might cross tissue planes.  Given the potential utility of radiographic extension across tissue planes in raising the differential of S anginosus , further research on the radiographic presentations of thoracic S anginosus is needed.

Advertisements

EUHM Report: Acute and subacute shortness of breath in patients with Pneumocystis Jirovecii Pneumonia

HIV-infected patients usually develop a subacute course of disease, while non-HIV infected immunocompromised patients are characterized by a rapid disease progression with higher risk of respiratory failure and higher mortality. The main symptoms usually include exertional dyspnea, dry cough, and subfebrile temperature or fever.

Salzer, Helmut J F, Guido Schäfer, Martin Hoenigl, Gunar Günther, Christian Hoffmann, Barbara Kalsdorf, Alexandre Alanio, and Christoph Lange. “Clinical, Diagnostic, and Treatment Disparities between HIV-Infected and Non-HIV-Infected Immunocompromised Patients with Pneumocystis Jirovecii Pneumonia.” Respiration. 96, no. 1 (2018): 52-65.

The diagnosis of PCP is mostly a presumptive diagnosis in resource-limited settings. Clinical signs and symptoms, particularly dyspnea, fever, dry cough, and hypoxia in absence of an alternative diagnosis in an immunocompromised patient with a CD4+ T lymphocyte count <200 cells/mL and concurrent radiological changes lead to the initiation of PCP treatment

Table 1. Disease characteristics of PCP in HIV-positive patients compared to patients with other reasons of immunosuppression (page 4)

 

 

VA Report: What is the relationship between uremia and altered mental status?

Measurement of the defects in mental function caused by uremia is also made difficult by the confounding effects of age, personal background, and other illnesses.  Not knowing which uremic solutes are toxic limits our ability to improve therapy. The contribution of retained solutes to the illness experienced by dialysis patients is difficult to dissect, but we believe it is large. We know that if dialysis is withheld, accumulation of waste solutes will cause confusion, coma, and then death.

Meyer TW, Hostetter TH. Approaches to Uremia. Journal of the American Society of Nephrology : JASN. 2014;25(10):2151-2158.

In studying the effects of uremia on mental function, we must also consider how much function will be improved by the reductions in solute levels we are able to achieve. It is worth considering what would be the effect on mental function of reducing levels of a known neuroactive compound, such as ethanol. Reducing very high ethanol levels by half could restore orientation in a stuporous person, analogous to the effect of initiating dialysis in a severely uremic patient.

Table 1.

Common features of uremia

Neural and Muscular                                         Endocrine and Metabolic
Loss of energy                                                            Amenorrhea and sexual dysfunction
Decreased mental acuity                                         Insulin resistancea
Anorexia and nausea                                                Reduced resting energy expenditure
Restless legs                                                               Increased protein/muscle catabolism
Defective taste and smell                                         Other
Peripheral neuropathy                                          Pruritus
Sleep disturbances                                                    Decreased red cell survivala
Reduced muscle membrane potential               Platelet dysfunctiona
Oxidant stressa

EUHM Report: What are the common presentations of hepatic abscess?

The Bottom Line: Most cases of hepatic abscess present at advanced age. One study reported a mean age > 57 years.19 This finding suggests that older individuals are more susceptible to bacterial infection and thus abscess formation.  Most of the symptoms of hepatic abscess are due to infection and are nonspecific and it can be quite difficult to diagnose in a timely manner.  The most commonly reported signs and symptoms (Table 2. Page 162) include fever in most but not all cases, abdominal pain, and hypotension

Mavilia, M. G., Molina, M., & Wu, G. Y. (2016). The Evolving Nature of Hepatic Abscess: A Review. Journal of Clinical and Translational Hepatology, 4(2), 158–168.

Hepatic abscess remains a serious and often difficult to diagnose problem. HAs can be divided into three main categories based on the underlying conditions: infectious, malignant, and iatrogenic. Infectious abscesses include those secondary to direct extension from local infection, systemic bacteremia, and intra-abdominal infections that seed the portal system.  Hepatic abscess can be defined as an encapsulated collection of suppurative material within the liver parenchyma, which may be infected by bacterial, fungal, and/or parasitic micro-organisms

VA Report: Why do some patients with heart failure experience severe sweating?

In Morgan and Nadas’s seminal study they reported that sweating was greater at rest in HF patients compared with controls. Moreover, recent studies suggest that HF patients have similar sweating responses to controls when exposed to passive wholebody heating (Table 1).

Table 1. A Summary of Findings From Key Studies to Date Examining Thermoregulation in the Context of HF

Balmain, B., Sabapathy, S., Jay, O., Adsett, J., Stewart, G., Jayasinghe, R., & Morris, N. (n.d.). Heart Failure and Thermoregulatory Control: Can Patients With Heart Failure Handle the Heat? Journal of Cardiac Failure., 23(8), 621-627.

A common finding among studies examining thermoregulation in the context of HF to date is that HF patients appear to demonstrate impaired heat-induced increases in SkBF compared with controls. Although the mechanisms responsible for impaired SkBF in HF are not yet well understood, it may be argued that the compensatory activation of neurohumoral mechanisms that increase with severity of the condition at least partially contribute to the blunted heat-induced rise in SkBF in HF patients

EUHM Report: What syndromes are associated with Pulse Temperature Disassociation?

The Bottom Line: The mechanisms for fever-induced bradycardia are not completely understood. It is well known that many infectious agents can cause acute myocarditis and induce cardiac conduction abnormalities. One study suggested that relative bradycardia due to a specific disease has no predictive value in making a diagnosis. However, another  suggests that relative bradycardia in a single patient can be helpful in arriving at a tentative diagnosis.

Mittal J, Estiverne C, Kothari N, Reddi A. Fever and Relative Bradycardia: A Case Presentation and Review of the Literature. Int J Case Rep Short Rev. 2015;1(1): 004-008.

In many noninfectious and infectious conditions, the heart rate does not increase with a rise in temperature. This phenomenon is called pulse-temperature deficit which many clinicians refer to as relative bradycardia. A caveat to this rule is that a patient must have a temperature of at least 102 F in order to better appreciate this pulse temperature relationship

EUH Dressler Conference: Review of polymyositis

The Bottom Line: Inflammatory idiopathic myopathies (IIM) are a group of rare autoimmune diseases characterized by proximal skeletal muscle weakness, raised muscle enzymes and extramuscular organ involvement, most frequently the lungs, resulting in interstitial lung disease (ILD). Numerous autoantibodies are associated with the disease, many linked to different clinical phenotypes.  Polymyositis predominantly presents with proximal symmetrical muscle weakness, while dermatomyositis is characterized by skin and muscle involvement; both are associated with extramuscular features.

Clark, K., & Isenberg, D. (n.d.). A review of inflammatory idiopathic myopathy focusing on polymyositis. European Journal of Neurology., 25(1), 13-23.

The main aims of treatment are to suppress inflammation, improve muscle power and prevent chronic damage to muscles and extramuscular organs. However, there is a lack of robust data to guide treatment.  Glucocorticoids remain the mainstay of treatment in IIM. Initial dosing is approximately 0.5 mg/kg of prednisolone, but the many side effects of steroids encourage a reducing regime over the first 2 months.  Methotrexate and azathioprine are often used as first line disease modifying anti-rheumatic drugs. A Cochrane review found insufficient evidence of improved efficacy using one DMARD (methotrexate, azathioprine or cyclosporine) in combination with corticosteroids in preference to another.

VA Report: Dysphagia in the setting of myocardial infarction

Examples for extrinsic esophageal compression are found in inflammatory, postoperative and neoplastic mediastinal diseases, but also in substernal strumae, cervical spondylitis and vertebral osteophytes. Vascular esophageal compression syndromes are typically caused by an aberrant origin of the right subclavian artery far left in the aortic branch and course of this “A. lusoria” anterior or posterior of the esophagus. In addition, similar forms of esophageal compression can result from a congenital right-sided aorta, aortic aneurysms and conditions of left atrial enlargement.

Werner, C., Rbah, R., & Böhm, M. (n.d.). Cardiovascular dysphagia. Clinical Research in Cardiology : Official Journal of the German Cardiac Society., 95(1), 54-56.

Radiological imaging revealed an extrinsic esophageal compression as the cause of the patient’s complaints, for example, due to a mediastinal tumor. However, computed tomography of the chest showed a rare case of cardiovascular compression as the cause of dysphagia in this case. The patient turned down the option of endoscopic examination at the time.

EUH Dressler Case Conference: Review of Myocardial Infarction and Myocardial Ischemia

The Bottom Line: Myocardial infarction (MI) is caused by prolonged myocardial ischemia, a condition where atherosclerotic plaques limit coronary flow reserve. About 25% of patients exhibiting symptoms of acute cardiac ischemia (ACI) will have a myocardial infarction.

References:

Lanza GA, Crea F. Overview of Management of Myocardial Ischemia: a Mechanistic-Based Approach. Cardiovasc Drugs Ther. 2016 Aug;30(4):341-349.

Simel DL, Goodacre SW, Kristin L. “Myocardial Infarction”. The Rational Clinical Examination: Evidence-Based Clinical Diagnosis. Eds. David L. Simel & Drummond Rennie. New York, NY: McGraw-Hill.

Diagnosing a patient with MI should be based on whether the patient is exhibiting symptoms (i.e. chest pain, shortness of breath, cardiac arrest, abdominal pain) rather than whether the patient exhibits any risk factors for MI. The most beneficial methods to detect acute myocardial infarction are by observing changes in the Q waves or observing ST-segment elevation or depression on an ECG by the bedside; if ECG results are normal or non-diagnostic, measuring the patient’s symptoms using predictive models can be useful in diagnosing MI.

 

VA Report: What is the etiology and treatment options for Rapidly progressive crescentic glomerulonephritis?

The Bottom Line:  Early treatment is of paramount importance for patients with crescentic GN. The current approach is based on a combination of corticosteroids and cytotoxic drugs with the aims of quenching the active inflammation and abating the cellular response and the antibody production

The etiology and the initial pathogenetic factors are different in the three types, but the final mechanisms leading to crescent formation and the renal symptoms and signs are similar.

Moroni, G., & Ponticelli, C. (n.d.). Rapidly progressive crescentic glomerulonephritis: Early treatment is a must. Autoimmunity Reviews, 13(7), 723-729.

The term crescentic glomerulonephritis (GN) refers to a pathologic condition characterized by extracapillary proliferation in > 50% of glomeruli. Clinically crescentic GN is characterized by a nephritic syndrome rapidly progressing to end stage renal disease (ESRD).