Beyond masks and hand hygiene, what factors impact transmission of Covid-19 in indoor gatherings?

Aside from factors specific to the source individual (eg, viral load in exhaled air, “superspreader” features, etc…) and host characteristics (eg, older age, obesity, immunocompromised state), transmission of SARS-CoV-2 in indoor settings may be impacted by several factors, including social distancing, ventilation of rooms/ direction of airflow, room occupancy, exposure time and higher risk activities, such as eating, talking loud, heavy breathing during exercise, laughing, coughing and sneezing. 1-4

  1. Physical distance from infected individuals. Although a “safe” distance of 6 feet has often been cited, increasing evidence suggests that SARS-CoV-2 may be spread not only by larger droplets but also by airborne route (ie, beyond 6 feet or shortly after an infected person leaves the area). In fact, 8 of 10 studies on horizontal droplet distance have reported droplets traveling more than 6 feet (2 meters), some cases up to 26 feet (8 meters), and 1 study documented virus at 13 feet (4 meters). Transmission beyond 6 feet is not surprising since even as early as 1948 beta streptococci were found 9.5 feet from 10% of people who were infected!1
  2. Quality of ventilation and direction of airflow in the room. Poorly ventilated rooms would be expected to have more potentially infectious droplets in the air for longer periods of time, even after an infected person leaves the area.
  3. Room occupancy. The higher the occupancy the more likely to have exhaled contaminated air from 1 or more infected persons (symptomatic or asymptomatic) with exposure of susceptible hosts.
  4. Exposure time. Exposure to contaminated air in the room even for a relatively short period of time (ie, >5-15 minutes) is likely to increase the risk of transmission.
  5. Activity of infected individual. Many activities such as singing, speaking loudly, eating, laughing, breathing heavily during exercise, coughing and sneezing may increase risk of Covid-19 transmission in indoor settings.

Recall that over one-half of Covid-19 transmissions are due to asymptomatic individuals.5 In this setting and in the presence of factors discussed above, it’s easy to see how transmission of Covid-19 in indoor settings can occur readily, possibly explaining cases without apparent source.

Bonus Pearl: Did you know that the odds of Covid-19 transmission may be 18.7 times greater indoors compared to open-air environment and the odds of superspreading event in closed environments may be 32.6 times higher?4

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References

  1. Bahl P, Doolan C, de Silva C, et al. Airborne or droplet precautions for health workers treating coronavirus disease 2019? J Infect Dis 2020. Published online April 16, 2020. https://pubmed.ncbi.nlm.nih.gov/32301491/
  2. Jones NR, Quereshi Z, Temple RJ, et al. Two metres or one: what is the evidence for physical distancing in covid-19? BMJ 2020;370:m3223. https://www.bmj.com/content/370/bmj.m3223/rr-18
  3. Johansson MA, Quandelacy TM, Kada S, et al. SARS-CoV-2 transmission from people without COVID-19 symptoms. JAMA Network open. 2021;4():e2035057. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2774707?utm_source=For_The_Media&utm_medium=referral&utm_campaign=ftm_links&utm_term=010721
  4. Nishiura H, Oshitani H, Kobayashi T, et al. Closed environments facilitate secondary transmission of coronavirus disease 2019 (COVID-19). MedRxiv 2020. https://www.medrxiv.org/content/10.1101/2020.02.28.20029272v2.full.pdf
  5. Leclerc QJ, Fuller NM, Knight LE,e tal. What settings have been linked to SARS-CoV-2 transmission clusters? Wellcome Open Research October, 2020. https://wellcomeopenresearch.org/articles/5-83    

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 or its affiliate healthcare centers. 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!

Beyond masks and hand hygiene, what factors impact transmission of Covid-19 in indoor gatherings?

Can the elevation of AST and ALT in my patient with rhabdomyolysis be related to the muscle injury itself?

Yes! Elevated serum AST and ALT in the setting of rhabdomyolysis is not uncommon and, at least in some cases, appears to be related to the skeletal muscle injury itself.1,2

In a study of 16 patients considered to have significant muscle necrosis due to extreme exercise, polymyositis or seizures without evidence of liver disease (eg, viral hepatitis, exposure to hepatotoxic drugs, heart failure, biliary tract disease, recent hypotension) AST and, to lesser degree, ALT was elevated. For extreme exercise, the median AST and ALT concentrations were 2,466 IU/L and 497 U/L, respectively, while for seizures these levels were 1,448 U/L and 383 U/L respectively.1  

Another study reported AST elevation (>40 U/L) in 93.1% of patients with rhabdomyolysis and ALT elevation (>40 U/L) in 75.0% of patients with serum creatine kinase ≥1000 U/L. Further supporting a skeletal muscle origin for AST elevation was the finding that AST concentrations fell in parallel with CK drop during the first 6 days of hospitalization for rhabdomyolysis. It was posited that ALT concentrations dropped slower because of its longer serum half-life (47 hours vs 17 hours for AST).2 Despite these findings, concurrent liver injury as an additional source of AST or ALT elevation cannot be excluded.

Elevation of AST and ALT with muscle injury should not come as a surprise. AST is found in heart and skeletal muscle among many other organs. Even ALT which is considered more specific to liver is found in organs such as skeletal muscle, heart and kidney, though at lower concentrations.3

Bonus Pearl: Did you know that the first description of rhabdomyolysis in the literature involved English victims of crush injuries during World War II?2

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References

  1. Nathwani RA, Pais S, Reynolds TB, et al. Serum alanine aminotransferase in skeletal muscle diseases. Hepatology 2005;41:380-82. https://www.ncbi.nlm.nih.gov/pubmed/15660433
  2. Weibrecht K, Dayno M, Darling C, et al. Liver aminotransferases are elevated with rhabdomyolysis in the absence of significant liver injury. J Med Toxicol 2010;6:294-300. https://link.springer.com/article/10.1007%2Fs13181-010-0075-9
  3. Giannini EG, Testa R, Savarino V. Liver enzyme alteration: a guidance for clinicians. CMAJ2005;172:367-79. Giannini EG, Testa R, Savarino V. Liver enzyme alteration: a guidance for clinicians. CMAJ 2005;172:367-79. https://www.ncbi.nlm.nih.gov/pubmed/15684121
Can the elevation of AST and ALT in my patient with rhabdomyolysis be related to the muscle injury itself?

What could be causing low serum haptoglobin in my patient with no evidence of hemolysis?

 

There are many causes of low serum haptoglobin besides hemolysis, including1-4:

  • Cirrhosis of the liver
  • Disseminated ovarian carcinomatosis
  • Pulmonary sarcoidosis
  • Elevated estrogen states
  • Repetitive physical exercise
  • Hemodilution
  • Blood transfusions
  • Drugs (eg, oral contraceptives, chlorpromazine, indomethacin, isoniazid, nitrofurantoin, quinidine, and streptomycin)
  • Iron deficiency anemia
  • Megaloblastic anemia (by destruction of megaloblastic RBC precursors in the bone marrow)
  • Congenital causes

Less well-known is that congenital haptoglobin deficiency (“anhaptoglobinemia”) may not be so rare in the general population at a prevalence of 1% among whites and 4% among African-Americans (>30% in blacks of West African origin)3. Measurement of serum hemopexin, another plasma protein that binds heme, may help distinguish between this condition and acquired hypohaptoglobinemia— in the absence of hemolysis, hemopexin levels should remain unchanged3,5.

Final Fun Fact: Did you know that serum haptoglobin is often low during the first 6 months of life?

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References

 

  1. Shih AWY, McFarane A, Verhovsek M. Haptoglobin testing in hemolysis: measurement and interpretation. Am J Hematol 2014;89: 443-47. https://www.ncbi.nlm.nih.gov/pubmed/24809098
  2. Sritharan V, Bharadwaj VP, Venkatesan K, et al. Dapsone induced hypohaptoglobinemia in lepromatous leprosy patients. Internat J Leprosy 1981;307-310. https://www.ncbi.nlm.nih.gov/pubmed/7198620
  3. Delanghe J, Langlois M, De Buyzere M, et al. Congenital anhaptoglobinemia versus acquired hypohaptoglobinemia. Blood 1998;9: 3524. http://www.bloodjournal.org/content/bloodjournal/91/9/3524.full.pdf
  4. Haptoglobin blood test. https://medlineplus.gov/ency/article/003634.htm. Accessed August 6, 2017.
  5. Smith A, McCulloh RJ. Hemopexin and haptoglobin: allies against heme toxicity from hemoglobin not contenders. Front. Physiol 2015;6:187. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485156/pdf/fphys-06-00187.pdf

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its 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 could be causing low serum haptoglobin in my patient with no evidence of hemolysis?