Author: FA Manian MD, MPH

Do proton pump inhibitors (PPIs) reduce the risk of bleeding from lower gastrointestinal tract?

FA Manian MD, MPH, , , , , , , , , , , , , , Leave a comment

The short answer is “No”!  Although proton pump inhibitors (PPIs) are effective in reducing the risk of upper gastrointestinal bleed (GIB) in high-risk patients, they do not protect against lower GIB. 1 In fact, their use has been associated with an increased risk of small bowel injury related to non-steroidal anti-inflammatory drugs (NSAIDs) and low-dose aspirin.2,3

A 2015 case-control study involving over 1,000 patients hospitalized for GIB found that although concomitant use of PPI in patients on NSAIDs, low-dose aspirin, other antiplatelet agents or anticoagulants was associated with a reduced risk of UGIB, it was not associated with reduced risk of lower GIB.  Interestingly, in this study, PPIs were associated with higher risk of lower GIB which might have been related to confounding factors and not necessarily a direct causal effect.4 Lack of an impact of PPIs on lower GIB among patients on aspirin or NSAIDS has also been supported by others. 5-7

The fact that PPIs don’t seem to reduce the risk of GIB distal to the duodenum should not be surprising given their primary mechanism of action through inhibition of acid production by gastric parietal cells. 8  What is perhaps more intriguing is how they may potentially increase the risk of small intestinal injury while still protecting the gastro-duodenum from NSAID-induced mucosal damage.

In a cool laboratory study involving rats, treatment with a PPI was associated with exacerbation of NSAID-induced intestinal ulceration and bleeding; by itself treatment with PPI was not associated with intestinal mucosa injury.9 Interestingly, in this study, a marked shifts in numbers and types of enteric bacteria with a significant reduction in jejunal Bifidobacteria spp was noted with PPI therapy. Restoration of small intestine Bifididobacteria during treatment with a PPI along with an NSAID prevented intestinal ulceration/bleeding. The investigators concluded that when used along with an NSAID, PPIs may cause small intestinal injury through alteration in the microbiome of the gut.  Fascinating!

Bonus Pearl: Did you know that the 2022 American Gastroenterological Association (AGA) clinical practice update on de-prescribing of PPIs lists several conditions for which acute/short term use of PPIs are NOT indicated, such as isolated lower GI symptomatology, acute nausea and vomiting not believed to be related to GERD/esophagitis, acute undifferentiated abdominal pain, and empiric treatment of laryngopharyngeal symptomatology? 10 

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

References

  1. Lue A, Lanas A. Proton pump inhibitor treatment and lower gastrointestinal bleeding: Balancing risks and benefits. World J Gastroenterol 2016;22:10477-10481. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5192259/#:~:text=PPIs%20do%20not%20prevent%20NSAID,and%20the%20risk%20of%20LGB.
  2. Endo H, Sakai E, Taniguchi L, et al. Risk factors for small-bowel mucosal breaks in chronic low-dose aspirin users: data from a prospective multicenter capsule endoscopy registry. Gastrointes Endosc 2014;80:826-34. https://pubmed.ncbi.nlm.nih.gov/24830581/
  3. Washio E, Esaki M, Maehata Y, et al. Proton pump inhibitors increase incidence of nonsteroidal anti-inflammatory drug-induced small bowel injury: A randomized, placebo-controlled trial. Clin Gastroenterol Hepatol 2016;14:809-815. https://pubmed.ncbi.nlm.nih.gov/26538205/
  4. Lanas A, Carrera-Lasfuentes P, Arguedas Y, et al. Risk of upper and lower gastrointestinal bleeding in patients taking nonsteroidal anti-inflammatory drugs, antiplatelet agents, or anticoagulants. Clin Gastroenterol Hepatol 2015;13:906-12. https://pubmed.ncbi.nlm.nih.gov/25460554/
  5. Nagata N, Niikura R, Aoki T, et al. Effect of proton-pump inhibitors on the risk of lower gastrointestinal bleeding associated with NSAIDs, aspirin, clopidogrel, and warfarin. J Gastroenterol 2015;50:1079-1086. https://pubmed.ncbi.nlm.nih.gov/25700638/
  6. Garcia Rodriguez LA, Lanas A, Soriano-Gabarro M, et al. Effect of proton pump inhibitors on risks of upper and lower gastrointestinal bleeding among users of low-dose aspirin: A population-based observational study. J Clin Med 2020;9:928. https://www.mdpi.com/2077-0383/9/4/928
  7. Casado Arroyo R, Polo-Tomas M, Roncales MP, et al. Lower GI bleeding is more common than upper among patients on dual antiplatelet therapy: long-term follow-up of a cohort of a patients commonly using PPI co-therapy. Heart 2012;98:718-723. https://pubmed.ncbi.nlm.nih.gov/22523056/
  8. Engevik AC, Kaji I, Goldenring JR. The physiology of the gastric parietal cell. Physiol Rev 2020;100:573-602. The Physiology of the Gastric Parietal Cell – PMC (nih.gov)
  9. Wallace JL, Syer S, Denou E, et al. Proton pump inhibitors exacerbate NSAID-induced small intestinal injury by inducing dysbiosis. Gastroenterology 2011;141:1314-22. https://www.gastrojournal.org/action/showPdf?pii=S0016-5085%2811%2900926-7
  10. Targownik LE, Fisher DA, Saini SD. AGA clinical practice update on de-prescribing of proton pump inhibitors: expert review. Gastroenterology 2022;162:1334-1342. https://www.gastrojournal.org/article/S0016-5085(21)04083-X/fulltext

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Do proton pump inhibitors (PPIs) reduce the risk of bleeding from lower gastrointestinal tract?

Is there any evidence that proton pump inhibitors (PPIs) benefit patients with acute pancreatitis?

FA Manian MD, MPH, , , , , , , , , , , , , Leave a comment

Despite their widespread use, there is no firm evidence that PPIs should be routinely prescribed in the treatment of acute pancreatitis (AP).1   In fact, current guidelines do not include the use of PPIs as standard therapy in  AP. 1-3

Although a 2023 systematic review and meta-analysis involving 6 randomized controlled trials and 3 cohort studies of patients with AP found a significant decrease in the rate of pancreatic pseudocyst formation in patients who received PPI, no significant difference in the rates of 7-day mortality, length of hospital stay, or acute respiratory distress syndrome was found when compared to control groups.3

Theoretically, PPIs may improve the course of AP through reduction in the incidence of stress-related upper GI hemorrhagic complications.  However, the incidence of such complications in AP is quite low, ranging from 1.2% to 14.5%, with great majority of cases (>85%) unrelated to peptic ulcer disease. 3,4  These findings may help explain why it has been difficult to show any benefit for use of PPIs in reducing the incidence of GI bleed in AP.3,5

Similarly, although PPIs have been shown to reduce secretin-stimulated bicarbonate secretion by the pancreas, the clinical significance of this finding in the overall course of AP—except perhaps a lower risk of pseudocysts—remains unclear.3 Parenthetically, experimental studies have reported contradictory results regarding the inhibition of pancreatic enzyme production by PPIs,  with omeprazole failing to suppress amylase release in isolated pancreatic acini while pantoprazole showing reduced amylase secretion in rats.3

It is also unclear how the reported anti-inflammatory effects of PPIs may benefit the clinical course of AP.3,6 What is clear is that any potential benefits of PPIs in AP should be weighed against their potential adverse effects, including the risk of nosocomial pneumonia, Clostridiodes difficile infection, and spontaneous bacterial peritonitis.7,8 

Bonus Pearl: Did you know that PPIs may not only inhibit acid production by gastric parietal cells but also interfere with bactericidal activity of neutrophils?  One potential mechanism is interference with proton pump-dependent H202 generation within lysosomes necessary to create a highly acidic and bactericidal environment. 9  Fascinating!

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

References

  1. Arvanitakis M, Dumonceau JM, Albert J, et al. Endoscopic management of acute necrotizing pancreatitis: European Society of Gastrointestinal Endoscopy (ESGE) evidence-based multidisciplinary guideline. Endoscopy 2018; 50:524-46. Endoscopic management of acute necrotizing pancreatitis: European Society of Gastrointestinal Endoscopy (ESGE) evidence-based multidisciplinary guideline – European Society of Gastrointestinal Endoscopy (ESGE)
  2. Crocket SD, Wani S, Gardner TB, et al. American Gastroenterological Association Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology 2018;154:1096-1101. American Gastroenterological Association Institute Guideline on Initial Management of Acute Pancreatitis (gastrojournal.org)
  3. Horvath IL, Bunduc S, Hanko B , et al. No evidence for the benefit of PPIs in the treatment of acute pancreatitis: a systematic review and meta-analysis. Scientific Reports 2023;13:2791. https://doi.org/10.1038/s41598-023-29939-S
  4. Rana SS, Sharma V, Bhasin Dk, et al. Gastrointestinal bleeding in acute pancreatitis: etiology, clinical features, risk factors and outcome. Tropical Gastroenterology 2015;36:31-35. http://www.tropicalgastro.com/articles/36/1/gastrointestinal-bleeding-in-acute.html
  5. Demcsak A, Soos A, Kincses L, et al. Acid suppression therapy, gastrointestinal bleeding and infection in acute pancreatitis-An international cohort study. Pancreatology 2020;20:1323-31.lyso https://www.sciencedirect.com/science/article/pii/S142439032030658X?via%3Dihub
  6. Hackert T, Tudor S, Felix K, et al. Effects of pantoprazole in experimental acute pancreatitis. Comparative Study 2010;8:551-7. https://pubmed.ncbi.nlm.nih.gov/20851132/
  7. Elzouki AB, Neffati N, Rasoul FA, et al. Increased risk of spontaneous bacterial peritonitis in cirrhotic patients using proton pump inhibitors. GE Port J Gastroenterol 2019; 26:83-89. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6454390/#:~:text=The%20result%20showed%20that%20PPI,medical%20literature%20confirm%20this%20association.
  8. Yibirin M, De Oliveira D, Valera R, et al. Cureus 2021;13:e12759/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7887997/#:~:text=The%20most%20likely%20explanation%20for,incidence%20of%20pneumonia%20%5B2%5D
  9. Ozatik O, Ozatik EY, Tesen Y, et al. Research into the effect of proton pump inhibitors on lungs and leukocytes. Turk J Gastroenterol 2021;32:1003-1011. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8975296/

 

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

Is there any evidence that proton pump inhibitors (PPIs) benefit patients with acute pancreatitis?

My newly-admitted patient has positive blood cultures for Staphylococcus aureus.  How long should his S. aureus bacteremia be treated?

FA Manian MD, MPH, , , , , , , , , , , , , , , Leave a comment

Because of the tendency of S. aureus bacteremia (SAB) to disseminate (eg, endocarditis, spinal epidural abscess, other metastatic infections), it should be treated with a minimum of 2 weeks of IV antibiotics following first repeat negative blood cultures, irrespective of the source of infection or rate of clinical improvement. 1-6

Beyond 2 weeks, the ultimate duration of parenteral antibiotics for treatment of SAB depends on several factors, including whether it is considered an “uncomplicated” or “complicated”. 1,2

Generally, uncomplicated SAB is defined as:

  • Negative results of follow-up blood culture at 2-4 days after bacteremia and
  • Clinical defervescence within 72 h of IV therapy and removal of the presumed focus of infection (eg, debridement of soft tissue infection or IV catheter) and
  • No evidence of metastatic infection among patients with catheter-related bloodstream infection or with primary bacteremia without evidence of endocarditis on transthoracic (TTE) or transesophageal echocardiogram (TEE) and
  • No endovascular foreign material (eg, prosthetic devices)

Patients not meeting the above criteria should be considered to have complicated SAB. Some studies have also reported primary bacteremia without obvious source and community-acquired SAB as risk factors for complications.4,6  

Even uncomplicated SAB should still receive at least 2 weeks of IV anti-staphylococcal therapy.  In a prospective observational study involving 111 patients with uncomplicated SAB, shorter course (<2 weeks) of IV antibiotic therapy was associated with significantly higher rate of relapse with a trend toward primary bacteremia associated with increased treatment failure.4

All other patients not considered to have an uncomplicated SAB, should receive extended antibiotic therapy (eg, 4-6 weeks or longer) depending on several factors, including clinical course and suspicion for a diagnosis of established metastatic disease (eg, endocarditis, spinal epidural abscess, etc…).  Continued parenteral antibiotic therapy is standard practice as there is insufficient data to support use of oral antibiotics in the treatment of complicated SAB before 4-6 weeks of therapy is completed.2

Standard practice in the treatment of SAB should also include an infectious disease (ID) consultation which has been associated with significantly reduced rates of mortality and risk of relapse.7

 Bonus Pearl: Did you know that SAB is associated with a mortality of 20-30% in developed countries despite antibacterial therapies and source control strategies? 1

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

References

  1. Lam JC, Stokes W. The golden grapes of wrath—Staphylococcus aureus bacteremia: A clinical review. Am J Med 2023, 136:19-26. https://pubmed.ncbi.nlm.nih.gov/36179908/
  2. Kimming A, Hagel St, Weis S, et al. Management of Staphylococcus aureus bloodstream infections. Frontiers in Medicine 2021; 7: Article 616524. https://www.frontiersin.org/articles/10.3389/fmed.2020.616524/full
  3. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 52:e18-e55. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/216060
  4. Chong YP, Moon SM, Bang KM, et al. Treatment duration for uncomplicated Staphylococcus aureus bacteremia to prevent relapse: Analysis of a prospective observational cohort study. Antimicrob Agents Chemother 2013;57:1150-56. https://pubmed.ncbi.nlm.nih.gov/23254436/
  5. Kuehl R, Morata L, Boeing C, et al. Defining persistent Staphylococcus aureus bacteremia: secondary analysis of a prospective cohort study. Lancet 2020;20: 1409-17. https://pubmed.ncbi.nlm.nih.gov/32763194/
  6. Fowler VG, Olsen MK, Corey R, et al. Clinical identifiers of complicated Staphylococcus aureus Arch Intern Med 2003;163:2066-72. https://pubmed.ncbi.nlm.nih.gov/14504120/
  7. Vogel M, Schmitz RPH, Hagel S, et al. Infectious disease consultation for Staphylococcus aureus bacteremia—A systematic review and meta-analysis. J Infect 2016, 72:19-28. https://pubmed.ncbi.nlm.nih.gov/26453841/ 

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My newly-admitted patient has positive blood cultures for Staphylococcus aureus.  How long should his S. aureus bacteremia be treated?

The urine culture of my female patient with urgency is growing Lactobacillus spp.  Should I treat it?

FA Manian MD, MPH, , , , , , , , Leave a comment

Lactobacillus spp. isolated from urine generally does not require treatment because these organisms are often part of the normal bacterial flora of the genitourinary (GU) and gastrointestinal tracts, are generally of low virulence, are rarely associated with urinary tract infections (UTIs) and may in fact have potential benefits in preventing UTIs. 1-4

In a study involving female urinary microbiome, subjects with urgency urinary incontinence were less likely to have Lactobacillus spp. based on 16S rRNA gene sequencing of transurethral catheter urine than those without symptoms, suggestive of possible protective role of this organism in female GU tract.1

Although Lactobacillus UTI is rare, one particular species, Lactobacillus delbrueckii, has been implicated in several case reports involving primarily elderly women.3,4

Vaginal colonization with lactobacilli provides a natural, nonspecific defense mechanism against infection in part by production of lactic acid and lowering of the regional pH which, when combined with hydrogen peroxide production by commensal anaerobes, interferes with colonization of the vaginal mucosal surfaces by potential pathogens. Lactobacilli also interfere with the adherence of pathogens by production of biosurfactants.3 It’s no surprise that lactobacilli are often considered “friendly bugs” and used in many probiotic preparations.

Bonus Pearl: Did you know that contrary to the current dogma, urine is not necessarily sterile.  Even in asymptomatic people, it may contain several organisms, including Lactobacillus, Gardnerella, Streptococcus, Staphylococcus (not aureus) and Corynebacterium? 5

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

  1. Pearce MM, Hilt EE, Rosenfeld AM, et al. The female urinary microbiome: a comparison of women with and without urgency urinary incontinence. mBio 2014;5:e01283-14. https://pubmed.ncbi.nlm.nih.gov/25006228/
  2. Thomas-White K, Forster SC, Kumar N, et al. Culturing of female bladder bacteria reveals an interconnected urogenital microbiota. Nature Communications 2018;9:1557. https://www.nature.com/articles/s41467-018-03968-5.pdf (urine not sterile, bladder with lactobacillus prevention, normal asymptomatic
  3. Darbro BW, Petroelje BK, Doern GV. Lactobacillus delbureckii as the cause of urinary tract infection. J Clin Microbiol 2009;47:275-277. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2620876/#:~:text=Urinary%20tract%20infections%20caused%20by,a%20setting%20of%20ureteral%20obstruction.
  4. Maillet F, Passeron A, Podglajen I, et al. Lactobacillus delbrueckii urinary tract infection in a male patient. Med Mal Infect 2019;49:225-230. https://www.sciencedirect.com/science/article/pii/S0399077X1830787X?via%3Dihub
  5. Reid G. The scientific basis for probiotic strains of Lactobacillus. App Env Microbiol 1999;65:3763-3766. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC99697/

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

The urine culture of my female patient with urgency is growing Lactobacillus spp.  Should I treat it?

Chest CT scan of my patient with congestive heart failure (CHF) and shortness of breath shows mediastinal adenopathy.  Can mediastinal adenopathy be caused by CHF alone?

FA Manian MD, MPH, , , , , , Leave a comment

Yes! Mediastinal adenopathy (commonly defined as 1 or more lymph nodes with a short axis diameter >1 cm) may be caused by CHF alone (AKA “congestive adenopathy”). 1-4

Although not as common as alveolar/interstitial edema on chest CT scan, hypertrophy of mediastinal lymph nodes may occur in a significant number of patients with CHF.  In a study involving 215 patients with CHF and no confounding etiology of adenopathy, 68% had evidence of adenopathy, particularly involving the right paratracheal and precarinal, subcarinal and other mediastinal lymph nodes; hilar and single station adenopathy were less common. The findings of pulmonary edema on CT and pleural effusion were significantly associated with adenopathy.1

In a study involving 3 patients with mediastinal adenopathy and CHF, lymph node biopsy showed noninflammatory, benign lesions that did not affect the node structure. Follow-up CT scan in 2 patients at 8 and 10 months showed no changes in the morphologic characteristics of mediastinal lymph nodes, while in another patient most of the enlarged lymph nodes disappeared at 5 months post- acute phase of the CHF.2   Interestingly, another study involving 31 cases of “subacute left heart failure” found that average ejection fraction was lower among patients with adenopathy (34% vs 43%).3

One potential mechanism for CHF-related adenopathy is that the excess lung fluid causes increased flow of fluid through the lymphatic channels and into the lymph nodes resulting in their congestion and enlargement.1

 

Bonus Pearl: Did you know that experimental animal studies have shown that acute CHF is associated with significant increases in mediastinal lymphatic flow and lymphatic vessel dilatation? 4-5

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

  1. Shweihat YR, Perry J, Etman Y, et al. Congestive adenopathy: A mediastinal sequela of volume overload. J Bronchol Intervent Pulmonol 2016; 23:298-302. https://pubmed.ncbi.nlm.nih.gov/27623420/
  2. Ngom A, Dumont P, Diot P, et al. Benign mediastinal lymphadenopathy in congestive heart failure. CHEST 2001;119: 653-656. https://pubmed.ncbi.nlm.nih.gov/11171755/
  3. Chabbert V, Canevet G, Baixas C, et al. Mediastinal lymphadenopathy in congestive heart failure: a sequential CT evaluation with clinical and echocardiographic correlations. Eur Radiol 2004;14:881-889. https://pubmed.ncbi.nlm.nih.gov/14689226/
  4. Drake RE, Dhother S, Teague RA, et al. Lymph flow in sheep with rapid cardiac ventricular pacing. Am J Physiol 1997; 272:1595-1598. https://pubmed.ncbi.nlm.nih.gov/9176352/
  5. Leeds SE, Uhley HN, Telesky LB. Direct cannulation and injection lymphangiography of the canine cardiac and pulmonary efferent mediastinal lymphatics in congestive hart failure. Invest Radiol 1981;16:193-200. https://pubmed.ncbi.nlm.nih.gov/6266975/

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Chest CT scan of my patient with congestive heart failure (CHF) and shortness of breath shows mediastinal adenopathy.  Can mediastinal adenopathy be caused by CHF alone?

Is there an association between Covid-19 and subsequent development of hypertension?

FA Manian MD, MPH, , , , , , , , , , , , Leave a comment

Although far from definite, emerging evidence suggests that adults with recently diagnosed Covid-19 are at increased risk of newly-diagnosed hypertension following the acute infection.1-4

A retrospective cohort study involving a large national healthcare data base of the Department of Veterans Affairs found that, at a median follow-up of 126 days, Covid-19 survivors had an excess burden of newly-diagnosed hypertension (15/1000 patients) and were at higher risk of initiation of antihypertensive drugs compared to controls.2

Another retrospective cohort study involving over 80,000 adults 65 years or older (median follow-up 56 days) found an increased risk of newly-diagnosed hypertension (O.R. 4.4; 95% C.I. 2.27-6.37) in the Covid-19 group. 3  Even in a younger population (18-65 years of age), the same investigators found a significant increase (81%; 95% C.I. 10-196%) in the risk of newly diagnosed hypertension in the Covid-19 group compared to that of the control cohort. 4  

Despite the inherent limitations in these retrospective studies, a cause-and-effect relationship between Covid-19 and subsequent diagnosis of hypertension is plausible given the known affinity of SARS-CoV-2 for ACE2 receptors and endothelial cells. 5   Of interest, hyperreninemia associated with reduced glomerular filtration rate has been reported in some patients with Covid-19 requiring prolonged intensive care. 6

Bonus Pearl: Did you know that Covid-19 survivors have also been reported to have an increased risk of stroke, transient ischemic attack, ischemic heart disease, pericarditis, myocarditis, heart failure, dysrhythmia, and thromboembolic disease, independently of pre-existing hypertension and other cardiovascular risk factors? 7

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

References

  1. Shibata S, Kobayashi K, Tanaka M, et al. Covid-19 pandemic and hypertension: an updated report from the Japanese Society of Hypertension project team on Covid-19. Hypertens Res 2022 Dec 23:1-12. COVID-19 pandemic and hypertension: an updated report from the Japanese Society of Hypertension project team on COVID-19 – PMC (nih.gov)
  2. Al-Aly Z, Xie Y, Bowe B. High-dimensional characterization of post-acute sequelae of Covid-19. Nature 2021;594:259-64. High-dimensional characterization of post-acute sequelae of COVID-19 – PubMed (nih.gov)
  3. Daugherty SE, Guo Y, Health K, et al. Risk of clinical sequelae after the acute phase of SARS-CoV-2 infection: retrospective cohort study. BMJ 2021;373:n1098. Risk of clinical sequelae after the acute phase of SARS-CoV-2 infection: retrospective cohort study | The BMJ
  4. Guney C, Akar F. Epithelial and endothelial expressions of ACE2:SARS-CoV-2 Entry Routes.  J Pharm Pharm Sci 2021;24:84-98 Epithelial and Endothelial Expressions of ACE2: SARS-CoV-2 Entry Routes – PubMed (nih.gov)
  5. Cohen K, Ren S, Health K, et al. Risk of persistent and new clinical sequelae among adults aged 65 years and older during the post-acute phase of SARS-CoV-2 infection: retrospective cohort study. BBMJ 2022;376:e068414. Risk of persistent and new clinical sequelae among adults aged 65 years and older during the post-acute phase of SARS-CoV-2 infection: retrospective cohort study – PubMed (nih.gov) 
  6. Hulstom M, von Seth M, Frithiof R. Hyperreninemia and low total body water may contribute to acute kidney injury in coronavirus disease 2019 patients in intensive care. J Hypertens 2020 May 28. Hyperreninemia and low total body water may contribute to acute kidney injury in corona virus disease 2019 patients in intensive care – PMC (nih.gov)
  7. Xie Y, Xu E, Bowe B, et al. Long-term cardiovascular outcomes of Covid-19. Nat med 2022;28:583-90. Long-term cardiovascular outcomes of COVID-19 – PMC (nih.gov)

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Is there an association between Covid-19 and subsequent development of hypertension?

Can I estimate the central venous pressure (CVP) of my patient with dyspnea at the bedside by using point of care ultrasound (POCUS)?

FA Manian MD, MPH, , , , , , , , , , , , Leave a comment

Absolutely! Not only can POCUS be used to estimate the CVP by measuring the jugular venous pressure (JVP), it may also be more reliable than the traditional—often challenging—visual method of looking for internal jugular (IJ) waveforms in the neck.1

To estimate the CVP by POCUS, first position the patient in a comfortable (usually semi-recumbent) position.   Select “vascular” (ie, high frequency) setting on your device (linear array probe for traditional ultrasound devices).  With the probe in the transverse plane (ie,  perpendicular to the IJ) and the orientation marker pointing to the right of the patient, slowly slide the probe cranially until the IJ appears to collapse during end-expiration, a point commonly referred to as the “meniscus” (CLIP 1 below). Measure the vertical distance between the meniscus and the sternal angle and, just as you would using the traditional method, add 5 cm (see limitation below) to calculate the height of the JVP, with values > 8 cm considered elevated (Figure 1 below).1,2,3

You can also look for the point of JVP collapse in the longitudinal axis by rotating the transducer 90° clockwise (CLIP 2 below).  Here, the shape of the IJ resembles a wine bottle with the collapsed portion or the tip of the tapered portion or triangle, representing the meniscus.3

A major limitation of estimating the CVP by visualization of JVP or by POCUS is the assumption that the distance between the right atrium and the sternal angle is constant at 5 cm.  It turns out that this distance may potentially vary among patients depending on their body habitus and position.4    A cool study from 2015, however, more accurately determined this distance by adjusted ultrasound views of the center of the right atrium. 5    Clearly, bedside estimation of CVP by POCUS will continue to be refined in the future. 

Bonus Pearl: Did you know that the traditional non-invasive method of estimating CVP by examining neck veins was first proposed in 1930 by Sir Thomas Lewis, a British cardiologist, who has been called the “father of clinical cardiac electrophysiology” and coined the terms “pacemaker,” “premature contractions,” and “auricular fibrillation”?6,7

 

Clip 1. Transverse visualization of the internal jugular vein (IJV) by using POCUS. The meniscus is the point of IJV collapse during end-expiration. 

 

Figure 1. Measurement of the jugular venous pressure (JVP) by POCUS. Add 5 cm (green arrow) to the distance between the meniscus (internal jugular collapse on the transverse view or tip of the tapering zone on the longitudinal view) and the sternal angle (red arrow).

Clip 2. Longitudinal visualization of the internal jugular vein (IJV) by using POCUS. The meniscus is the tip of the tapering zone or triangle of the IJV. 

 

 

 

Contributed by Woo Moon D.O., Mercy Hospital, St. Louis, Missouri

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

1. Wang L, Harrison J, Dranow E, Aliyev N, Khor L. Accuracy of ultrasound jugular venous pressure height in predicting central venous congestion. Ann Intern Med 2021; 175:344-51.

2. McGee MD S. Evidence-Based Physical Diagnosis. 5th ed. Philadelphia: Elsevier; 2021.

3. Lipton B. Estimation of central venous pressure by ultrasound of the internal jugular vein. Am J Emerg Med 2000;18(4):432–4.

4. Istrail, L. POCUS and the jugular venous pressure: A deep dive. POCUS Med Ed, November 12. 2021. POCUS and the Jugular Venous Pressure: A Deep Dive (pocusmeded.com)

5. Xing C-Y, Liu Y-L, Zhao M-L, et al. New method for nonivasive quantification of central venous pressure by ultrasound. Circulation: Cardiovascular Imaging 2015;8/ https://doi.org/10.116/CIRCIMAGING.114.003085. New Method for Noninvasive Quantification of Central Venous Pressure by Ultrasound (ahajournals.org)

6. Sir Thomas Lewis – the Father of clinical cardiac electrophysiology | SciHi Blog [Internet]. [cited 2023 Feb 2]; Available from: http://scihi.org/thomas-lewis-cardiac-electrophysiology/

7. Lewis T. Remarks on early signs of cardiac failure of the congestive type. Br Med J 1930;1(3618):849–52.

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Can I estimate the central venous pressure (CVP) of my patient with dyspnea at the bedside by using point of care ultrasound (POCUS)?

What are the major changes in the 2023 evaluation and management (E/M) coding guidelines affecting the hospitalists?

FA Manian MD, MPH, , , , , , , Leave a comment

One of the biggest changes in the 2023 E/M guidelines will be a shift away from billing by history and physical exam to code levels that are now based on medical decision making and time, matching the previous documentation update for ambulatory services made in 2021.1

Along the same line, clinicians are no longer required to document a certain number of systems, past medical and family history and other information that may not be immediately relevant to active patient problems.  A “medically appropriate history and physical” is still required but it no longer has a role in code selection. If you use time-based billing, you are no longer required to document just the time spent on counseling and/or coordination of care but make sure to document all the work you performed on the date of the encounter.

Another notable change is collapsing of the observation CPT codes into the inpatient codes, so you should bill the same code for patients regardless of whether they are inpatient or observation.

The Medical Decision Making (MDM) table is also shifting to align with the office/outpatient table. Recall that the MDM is comprised of 3 domains: 1. Number and complexity of problems addressed at the encounter; 2. Amount and/or complexity of data to be reviewed and analyzed: and 3. Risk of complications and/or morbidity or mortality of patient management (for further information see also a relate Pearl).

One good thing that may come out of these changes is a move away from unnecessary “note bloat” with several pages that usually has very little relevance to the active patient problems or what is actually done each day.  Hopefully, these changes will encourage providers to better document their medical decision making, and the time spent doing it.

In short, when writing your notes, make sure you clearly address the most important question: “What did I do for this patient today?” 1

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

Reference

  1. Quinn R. E/M coding changes for 2023. The Hospitalist 2023; 27: 10. E/M Coding Changes for 2023 – The Hospitalist (the-hospitalist.org)

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What are the major changes in the 2023 evaluation and management (E/M) coding guidelines affecting the hospitalists?

Why Does My Young Female Patient Have Recurrent Spontaneous Pneumothoraces?

FA Manian MD, MPH, , , , , , , , , , , , Leave a comment

Causes of spontaneous pneumothorax are legion, including cigarette use, genetic predisposition, or most commonly subpleural bleb rupture. 1 However, in cases without an apparent cause, a young female patient with recurrent spontaneous pneumothorax should routinely be asked about the timing of the pneumothorax in relation to her menstrual periods.  If related, catamenial pneumothorax (CP)— also known as menses-associated pneumothorax—should also be considered.  

CP is commonly defined as 2 or more episodes of spontaneous pneumothoraces occurring within 72 hours of onset of menstruation. 2, 3 Classically, CP occurs in females between the ages of 30-40 years with a history of endometriosis and recurrent right-sided pneumothorax.

As for potential mechanisms to explain catamenial pneumothorax, several theories have been proposed, including the passage of air through the vagina and uterus during times of decreased cervical mucus production and peritoneal cavity into the pleural space via diaphragmatic fenestrations. 3 Another potential mechanism is the retrograde migration of endometrial tissue from the uterine lining via the right paracolic gutter into the pleural space through defects in the diaphragm. Endometrial necrosis following monthly cycles may then create air blebs and pneumothorax. 3,4 Although CP is the most common presentation of thoracic endometriosis, a diagnosis of endometriosis is not required for its diagnosis.3, 5

Initial evaluation of CP often includes chest X-ray, CT, or MRI which may show not only pneumothorax but also diaphragmatic nodules or fenestrations; CA-125 levels may also be elevated in CP due to endometriosis. 2,3,9  Endometriosis-related CP is diagnosed via video-assisted thoracoscopic surgery (VATS).  

Treatment includes surgical and medical options but, ultimately, the goal is to prevent recurrence which is more likely in CP compared to other pneumothoraces. 3, 6 Surgical approaches such as VATS, pleurodesis, and diaphragmatic plication or repair with mesh, may be considered but recurrence rates (8-40%) are common. 3,7 Treatment options also include hormone-suppression therapy resulting in atrophy of ectopic endometrial glands (eg, estrogen-progesterone oral contraceptives and gonadotropin-releasing-hormone [GNRH] agonists such as leuprolide). 2, 7

Bonus Pearl: Did you know that a condition called catamenial epilepsy also clusters around menstruation due to the diminished protective effect of progesterone against seizures?  10

Contributed by Mariam Krikorian, Medical Student (Lincoln Memorial University) Mercy Hospital-St. Louis

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

References

  1. Sahn, Steven A., Heffer, John E. Spontaneous Pneumothorax. N Engl J Med. 2000;342:858-874. https://www-nejm-org.lmunet.idm.oclc.org/doi/10.1056/NEJM200003233421207?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed.
  2. Haga, T., Kumasaka, T., Kurihara, M, etal. Immunohistochemical Analysis of Thoracic Endometriosis. Path Intl, 2013;63(9);429-434. https://onlinelibrary.wiley.com/doi/10.1111/pin.12089.
  3. Visouli, A. N., Zarogoulidis, K., Kougioumtzi, I., etal. Catamenial Pneumothorax. J Thora Dis. 2014;6(4). https://jtd.amegroups.com/article/view/3205/html.
  4. Rousset-Jablonski, C., Alifano, M., Plu-Bureau, G., etal. A. Catamenial Pneumothorax and Endometriosis-Related Pneumothorax: Clinical Features and Risk Factors. Mol Hum Reprod. 2011;26(99);2322-2329. https://academic.oup.com/humrep/article/26/9/2322/720483.
  5. Korom, S., Canyurt, H., Missbach, A., etal. Catamenial Pneumothorax Revisited: Clinical Approach and Systematic Review of the Literature. J Thorac Cardiovasc Surgery. 2004;128(4);502-508. https://www.jtcvs.org/article/S0022-5223(04)00772-X/fulltext.
  6. Haga, T., Kurihara, M., Kataoka, H., etal. Clinical-Pathological Findings of Catamenial Pneumothorax: Comparison Between Recurrent Cases and Non-Recurrent Cases. Ann Thorac. 2014;202(6);202-206. https://www.jstage.jst.go.jp/article/atcs/20/3/20_oa.12.02227/_article.
  7. Leong, A. C., Coonar, A. S., Lang-Lazdunski, L. L. Catamenial Pneumothorax: Surgical Repair of the Diaphragm and Hormone Treatment. Ann R Coll Surg Engl. 2006;88(6). https://publishing.rcseng.ac.uk/doi/10.1308/003588406X130732.
  8. Marjański, T., Sowa, K., Czapla, A., etal. Catamenial Pneumothorax – A Review of the Literature. Polish Journal of Thoracic and Cardiovascular Surgery. 2016;13(2);117-121. https://www.termedia.pl/Catamenial-pneumothorax-a-review-of-the-literature,40,27920,0,1.html.
  9. Bagan, P., Le Pimpec Barthes, F., Assouad, J, etal. Catamenial Pneumothorax: Retrospective Study of Surgical Treatment. Ann Thorac. 2022;75(22);378-381. https://www.annalsthoracicsurgery.org/article/S0003-4975(02)04320-5/fulltext.
  10. Herzog, Andrew. Catamenial Epilepsy: Definition, Prevalence, Pathophysiology and Treatment. Elsevier Sci. 2008;17;151-159. https://pubmed-ncbi-nlm-nih-gov.lmunet.idm.oclc.org/18164632/.

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Why Does My Young Female Patient Have Recurrent Spontaneous Pneumothoraces?

Is loss of sense of smell or taste much less common in Omicron-related Covid-19 compared to earlier strains of SARS-CoV-2?

FA Manian MD, MPH, , , , , , , , , , , , Leave a comment

Absolutely! Although loss of smell was a cardinal symptom of Covid-19 with earlier strains of SARS-CoV-2 (eg, Wuhan, alpha, delta), on average omicron causes olfactory dysfunction in only 13% of patients, 3-4 times lower than the earlier strains.1

But why is omicron less likely to causes loss of smell or taste? There may be at least 2 explanations. First explanation revolves around the solubility of omicron in the olfactory mucus. Recall that to access the olfactory epithelium, viruses and other pathogens have to first dissolve in and penetrate the mucus layer that not only allows odorants to reach the olfactory receptors but also protects the olfactory epithelium from toxins and pathogens. Hydrophilic and acid proteins can penetrate the mucus barrier more easily because they are more soluble in the mucus layer.1

What does this have to do with omicron? Well, it turns out that omicron with all its mutations in the spike protein is actually more alkaline than the Wuhan and delta strains. This means that omicron may have lower solubility in mucus and have a harder time reaching and infecting the olfactory epithelium. 1 Since the composition of olfactory mucous differs significantly from other mucus layers in the respiratory tract, omicron may still cause disease.2

Another potential mechanism may be related to the inefficiency of omicron in other steps necessary to infect nonneuronal cells of the olfactory epithelium within the nasal cavity, such as the endosomal route. 1 It turns out that cells of the olfactory epithelium express less of the endosomal membrane fusion proteases (cathepsins) which omicron prefers for cell entry! Fascinating! 

Bonus Pearl: Did you know that only 5-10% of functional olfactory neurons are required for a relatively normal sense of smell? This means that SARS-CoV-2 needs to eliminate at least 90% of all support cells of the olfactory neurons within a 3-4 day period (before their regeneration) for the host to notice anosmia?

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

References

  1. Butowt R, Bilinska K, von Bartheld C. Why does the omicron variant largely spare olfactory function? Implications for the pathogenesis of anosmia in coronavirus disease 2019. J Infect Dis 2022;226:1304-1308. Why Does the Omicron Variant Largely Spare Olfactory Function? Implications for the Pathogenesis of Anosmia in Coronavirus Disease 2019 – PubMed (nih.gov)
  2. Yoshikawa K, Wang H, Jaen C, et al. The human olfactory cleft mucus proteome and its age-related changes. Sci Rep 2018;8:17170. The human olfactory cleft mucus proteome and its age-related changes – PMC (nih.gov)
  3. Harding JW, Getchell TV, Margolis FL. Degeneration of the primary olfactory pathway in mice. V. Long-term effect of intranasal ZNS04 irrigation on behavior, biochemistry and morphology. Brain Res 1978;140:271-85. Denervation of the primary olfactory pathway in mice. V. Long-term effect of intranasal ZnSO4 irrigation on behavior, biochemistry and morphology – PubMed (nih.gov)

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Is loss of sense of smell or taste much less common in Omicron-related Covid-19 compared to earlier strains of SARS-CoV-2?