My patient with pulmonary embolism also reports new-onset hiccups. Are the two conditions related?

Hiccups (AKA singultus) are due to the involuntary contraction of the inspiratory muscles, especially the diaphragm. The hiccup reflex involves an afferent limb ( eg, the phrenic and vagus nerves, sympathetic fibers from T6-T12,  brainstem) and an efferent limb, primarily the phrenic nerve1,2.  Thus, the irritation of any part of the arc in the head, neck, chest, or abdomen may potentially lead to hiccups.

Conditions involving the chest cavity that may be associated with hiccups include lung cancer, GERD, herpetic esophagitis, myocardial ischemia, bronchitis, empyema, lung masses, pneumonia, pleuritis, and pacemaker lead injury 1-3.

Reports of patients with PE and persistent hiccups (lasting longer than 48 h) have also appeared in the literature1,3. Of interest, in a report involving 3 patients, 2 had submassive or “large” PE, with one displaying the classic EKG changes of S1Q3T3; the size of PE in another was not reported1.  In another case report, PE was “not small” and involved the anterior and lateral lower lobe segments of pulmonary artery2.  Although the exact mechanism of PE causing hiccups is not clear, irritation of the afferent or efferent limb of the reflex arc in the chest has been postulated.  

References

  1. Hassen GW, Singh MM, Kalantari H, et al. Persistent hiccups as a rare presenting symptom of pulmonary embolism. West J Emerg Med 202;13:479-483.
  2. Durning SJ, Shaw DJ, Oliva AJ et al. Persistent hiccups as the presenting symptom of a pulmonary embolism. Chest Disease Reports 2012;2:e2.
  3. Buyukhatipoglu H, Sezen Y, Yildiz A, et al. Hiccups as a sign of chronic myocardial ischemia. S Med J 2010;103: 1184-85.
My patient with pulmonary embolism also reports new-onset hiccups. Are the two conditions related?

What causes the “tree-in-bud” (TIB) opacities on the chest CT images of my patient with cough?

TIB opacities represent a normally invisible branches of the bronchiole tree (≤1 mm in diameter) that are severely impacted with mucous, pus, or fluid, with resultant dilatation and “budding” of the terminal bronchioles ( ≥2 mm in diameter)1 (photo).

Although initially described in 1993 as a thin-section chest CT finding in active tuberculosis, TIB opacities are by no means restricted to a specific lung entity, and may be of infectious as well as non-infectious causes.

TIB is most commonly seen with infectious bronchiolitis caused by bacteria (particularly Staphylococcus aureus, Hemophilus influenzae), mycobacteria (including atypical mycobacteria), viruses (eg, respiratory syncytial virus, cytomegalovirus), and fungi (eg, Pneumocystis jirovecii, Aspergillus sp.)1,2.

Non-infectious causes include inhalation of toxic gases, connective tissue disorders (eg, rheumatoid arthritis, Sjögren syndrome), cystic fibrosis, Kartagener syndrome, and non-infectious bronchiolitis (eg, obliterative bronchiolitis). Malignancy-related causes include chronic lymphocytic leukemia and pulmonary tumor embolism in breast, liver, kidney, stomach, prostate and ovarian cancers3.

References

  1. Collins J, Blankenbaker D, Stern EJ. Ct patterns of bronchiolar disease: What is “tree-in’bud”? AJR 1998;171:365-70.
  2. Rossi SE, Franquet T, Volpacchio M, et al. Tree-in-bud pattern a t thin-section CT of the lungs: radiologic-pathologic overview. RadioGraphics 2005;25:789-801.
  3. Terhalle E, Gunther G. “Tree-in-bud”: thinking beyond infectious causes. Respiration 2015;89:162-165.

 

 

Photo: TIB opacities in a 50 year old man with productive cough and shortness of breath caused by infectious bronchiolitis.

treeinbud

 

What causes the “tree-in-bud” (TIB) opacities on the chest CT images of my patient with cough?

What is the significance of Howell-Jolly bodies (HJBs) in the peripheral smear of my patient with a spleen who presented with a pneumonia?

HJBs (Figure) are named after Henry Howell, an American physiologist who pioneered the use of heparin as an anti-coagulant and Justin Jolly, a French hematologist who filmed mitotic activity in cells. HJBs are nuclear remnants in circulating mature red blood cells which are usually pitted by the spleen under normal physiological conditions. They are often indicative of asplenia (either post-splenectomy or congenital absence) or hyposplenism associated with a variety of conditions, including  sickle cell disease, autoimmune disorders, celiac disease, inflammatory bowel disease, HIV, cirrhosis, primary pulmonary hypertension, splenic irradiation, amyloidosis, sarcoidosis, bone marrow transplantation, and high-dose corticosteroid therapy1-3.

Patients with pneumonia and HJBs on peripheral smear may be hyposplenic and at risk of potentially serious infections, predominantly caused by encapsulated bacteria eg, Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitidis3.  Such patients should be immunized against these organisms, including sequential receipt of both conjugated and polysaccharide pneumococcal vaccines3,4.

howelljollymgh

Photo courtesy of Michael S. Abers, MD

 

References

  1. Di Sabatino, A, Carsetti R, Corazza G. Post-splenectomy and hyposplenic states. Lancet 2011;378:86–97.
  2. Brousse, V, Buffet P, Rees D. The spleen and sickle cell disease: the sick(led) spleen. Br J Haematol 2014;166: 165–176.
  3. Mathew H, Dittus C, Malek A, Negroiu A. Howell-Jolly bodies on peripheral smear leading to the diagnosis of congenital hyposplenism in a patient with septic shock. Clin Case Rep 2015;3:714-717.
  4. Kuchar E, Miśkiewicz K , Karlikowska M. A review of guidance on immunization in persons with defective or deficient splenic function. Br J Haematol 2015; 171:683-94. doi: 10.1111/bjh.13660, Epub 2015 Aug 28.

Contributed by Katarzyna Orlewska, Medical Student, Warszawski Uniwersytet Medyczny, Poland

What is the significance of Howell-Jolly bodies (HJBs) in the peripheral smear of my patient with a spleen who presented with a pneumonia?

What is the sensitivity of nose swabs in detecting methicillin-resistant Staphylococcus aureus (MRSA) pneumonia?

In MRSA pneumonia, the sensitivity of nasal swab PCR may vary from as low as 24.2% to 88% (1-3). A single center  study involving  patients with possible healthcare-associated pneumonia (HCAP) and a low clinical pulmonary infection score (CPIS) — for whom antibiotics may not be necessary anyway (4)—suggested that discontinuation of empiric vancomycin in patients without an adequate respiratory culture and a negative nose and throat culture may be reasonable (5).  However, a prospective study of ICU patients concluded that “clinicians cannot reliably use the results of initial negative MRSA nasal swab results to withhold empirical MRSA coverage from patients who otherwise are at risk for MRSA infection” (3).

Thus, there is currently insufficient data to support discontinuation of vancomycin based on a negative nasal screen alone, particularly in patients who may be at high risk of MRSA pneumonia.

 

References

  1. Rimawi RH, Ramsey KM, Shah KB, et al. Correlation between methicillin-resistant Staphylococcus aureus nasal sampling, and S. aureus pneumonia in the medical intensive care unit. Infect Control Hosp Epidemiol 2014;35:590-92.
  2. Dangerfield B, Chung A, Webb B, et al. Predictive value of methicillin-resistant Staphylococcus aureus (MRSA) nasal swab PCR assay for MRSA pneumonia. Antimicrob Agents Chemother 2014;58:859-64.
  3. Sarikonda KV, Micek ST, Doherty JA, et al. Methicillin-resistant Staphylococcus aureus nasal colonization is a poor predictor of intensive care unit-acquired methicillin-resistant Staphylococcus aureus infections requiring antibiotic treatment. Crit Care Med 2010;38:1991-1995.
  4. Napolitano LM. Use of severity scoring and stratification factors in clinical trials of hospital-acquired and ventilator-associated pneumonia. Clin Infect Dis 2010;51:S67-S80.
  5. Boyce JM, Pop O-F, Abreu-Lanfranco O, et al. A trial of discontinuation of empiric vancomycin therapy in patients with suspected methicillin-resistant Staphylococcus aureus health care-associated pneumonia. Antimicrob Agents Chemother 2013;57:1163-1168.
What is the sensitivity of nose swabs in detecting methicillin-resistant Staphylococcus aureus (MRSA) pneumonia?

What is the utility of pulmonary auscultation for crackles (rales) in diagnosing congestive heart failure (CHF) or pneumonia?

The evidence for the accuracy of crackles in CHF is not as robust as often assumed, with wide variations in its sensitivity (13%-70%), specificity (35%-100%), positive predictive value (19%-100%), and negative predictive value (17%-85%) (1). In a study  of patients at high risk for CHF but without valvular heart disease, symptoms of CHF, or comorbid pulmonary disease,  the prevalence of baseline crackles in one or both lungs increased with age: 45-64 y , 11%; 65-79 y, 34%; and 80-95 y, 70%.  Overall, an at best fair or poor negative likelihood ratios (LRs) have been reported for crackles in CHF (3.4, and 0.8, respectively)(2). 

The accuracy of crackles in diagnosing pneumonia in patients with cough and fever is not much better: sensitivity 19-67%, specificity 36-94%, and poor positive and negative LRs (1.8 and 0.8, respectively) (2).

So don’t overestimate the accuracy of crackles in CHF or pneumonia!

  1. Kataoka H, Matsuno O. Age-related pulmonary crackles (rales) in asymptomatic cardiovascular patients. Ann Fam Med 2008;6:239-245.
  2. McGee S. Auscultation of the lungs. In Evidence-based physical diagnosis (3rd ed.). Elsevier Saunders, Philadelphia, 2012.
What is the utility of pulmonary auscultation for crackles (rales) in diagnosing congestive heart failure (CHF) or pneumonia?

What’s the latest on vaccination of adults 65 years old or over with conjugated pneumococcal vaccine?

Since August, 2014, the Advisory Committee on Immunization Practices (ACIP) has recommended routine use of 13-valent pneumococcal conjugated vaccine (PCV13, Prevnar) in adults ≥ 65 years, in addition to the traditional 23-valent pneumococcal polysaccharide vaccine (PPSV23, Pneumovax) (1).   The approval of PCV13 was based on a large randomized, double-blind, placebo-controlled trial (CAPITA) that found PCV13 effective in preventing vaccine-type pneumococcal, bacteremic, and nonbacteremic community-acquired pneumonia and vaccine-type invasive pneumococcal disease (2).

Due to the potential  for mutual interference with immunogenecity, these 2 vaccines should be spaced apart. When PPSV23 is administered first, PCV13 should be held for 1 year or longer. On the other hand, when PCV13 is administered first, PPSV23 can be given within 6-12 months (minimum 8 weeks). So it makes sense to give PCV13 first in our older pneumococcal vaccine-naive patients.

 

1. Tomczyk S, Bennett NM, Stoecker C, et al. Use of 13-valent pneumococcal conjuage vaccine and 23-valent penumococcal polysaccharide vaccine among adults aged ≥65 years: recommendations of the Advisory Committe on Immunization Practices (ACIP). MMWR;2014:63: 822-25.

2. Bonten MJM, Huijts, M, Bolkenbaas C, et al. Polysaccharide conjugate vaccine against pneumococcal pneumonia in adults. N Engl J Med 2015;372:1114-25.

 

What’s the latest on vaccination of adults 65 years old or over with conjugated pneumococcal vaccine?

Should corticosteroids (CS) be routinely considered in the treatment of hospitalized patients with community-acquired pneumonia (CAP)?

There has been much recent interest in the potential benefits of CS as adjunctive therapy to antibiotics in CAP. A recent systematic review on the subject concluded that for hospitalized adults with CAP, systemic CS may reduce mortality by about ~3% (primarily in severe CAP), mechanical ventilation need by ~5%, and hospital stay by ~1 day (1). But determining who might benefit the most and at what CS dosage regimen without undue risk of side effects (e.g. hyperglycemia) may be tricky.  

A randomized control trial of patients with CAP on prednisone 50 mg daily x 7d (vs placebo) showed a significant shorter time to clinical stability (3 vs 4.4 d) and higher in-hospital hyperglycemia in the CS group (2).; this study was not powered to detect significant difference in mortality, however.  Less treatment failure with adjunctive CS but without impact on mortality was recently reported in a small study involving patients with serum CRP >150 mg/L (i.e. high inflammatory state) (3).

Fortunately, a multicenter trial (ESCAPe, Extended Steroid in CAP) is currently underway. In the meantime, before considering CS, we need to be confident of the diagnosis and severity of CAP, its potential adverse effects in individual patients, and the appropriateness of the antibiotic (s) on board.

1. Siemieniuk RAC, Meade MO, Alonso-Coello P, et al. Corticosteroid therapy for patients hospitalized with community-acquired pneumonia: a systematic review and meta-analysis. Ann Intern Med 2015;165:519-528.

2. Blum CA, Nigro N, Briel M. Adjunct prednisone therapy for patients with community-acquired pneumonia: a multi-centre, double-blind randomized, placebo-controlled trial. Lancet 2015;385:1511-1518.

3. Torres A, Sibila O, Ferrer M, et al. Effect of corticosteroids on treatment failure among hospitalized patients with severe community-acquired pneumonia and high inflammatory response: a randomized clinical trial. JAMA 2015;313:677-86.

Should corticosteroids (CS) be routinely considered in the treatment of hospitalized patients with community-acquired pneumonia (CAP)?