This site is intended for healthcare professionals

Go to /sign-in page

You can view 5 more pages before signing in

COVID - summary of COVID-19 rapid guideline: managing the long-term effects of COVID-19 (long COVID)

Authoring team

This is a summary of the NICE guideline relating to:

  • new and emerging condition, which has been described using a variety of terms including ’long COVID’,
  • this condition can have a significant effect on people’s quality of life
  • there is no clinical definition or clear treatment pathway, and there is a minimal, though evolving, evidence base

The clinical case definitions, the term ’long COVID’ is commonly used to describe signs and symptoms that continue or develop after acute COVID-19.

  • Three definitions were developed (1):

    • acute COVID-19 (0 to 4 weeks),

    • ongoing symptomatic COVID-19 (4 to 12 weeks) and

    • post-COVID-19 syndrome (12 weeks or longer)

* the Office for National Statistics estimate that one in five people have symptoms that persist after 5 weeks, and one in ten have symptoms for 12 weeks or longer after acute COVID-19 infection (2)

NICE guidelines on managing the long term effects of covid-19 and the CDC define long covid patients or covid long haulers as individuals with ongoing symptoms of covid-19 that persist beyond four weeks from initial infection (3).

The panel of UK doctors who contributed to the article by Gorn et al (2) have provided a list of conditions, never experienced before their episodes of acute
COVID-19

Panel: Conditions experienced by members of the UK doctors #longcovid group

  • Myocarditis or pericarditis
  • Microvascular angina
  • Cardiac arrhythmias, including atrial flutter and atrial fibrillation
  • Dysautonomia, including postural orthostatic tachycardia syndrome
  • Mast cell activation syndrome
  • Interstitial lung disease
  • Thromboembolic disease (pulmonary emboli or cerebral venous thrombosis)
  • Myelopathy, neuropathy, and neurocognitive disorders
  • Renal impairment
  • New-onset diabetes and thyroiditis
  • Hepatitis and abnormal liver enzymes
  • New-onset allergies and anaphylaxis
  • Dysphonia

Crook et al have described the long term sequalae of covid-19

  • (1) in the alveoli of the lungs:
    • chronic inflammation
      • results in the sustained production of pro-inflammatory cytokines and reactive oxygen species (ROS) which are released into the surrounding tissue and bloodstream
    • endothelial damage
      • triggers the activation of fibroblasts, which deposit collagen and fibronectin resulting in fibrotic changes
    • endothelial injury, complement activation, platelet activation, and platelet-leukocyte interactions, release of pro-inflammatory cytokines, disruption of normal coagulant pathways, and hypoxia
      • may result in the development of a prolonged hyperinflammatory and hypercoagulable state, increasing the risk of thrombosis
  • (2) in the heart:
    • chronic inflammation of cardiomyocytes
      • can result in myositis and cause cardiomyocytes death
    • dysfunction of the afferent autonomic nervous system
      • can cause complications such as postural orthostatic tachycardia syndrome
    • prolonged inflammation and cellular damage prompts fibroblasts to secrete extracellular matrix molecules and collagen, resulting in fibrosis
    • fibrotic changes are accompanied by an increase in cardiac fibromyoblasts
      • damage to desmosomal proteins results in reduced cell-to-cell adhesion
  • (3) in the central nervous system:
    • long term immune response
      • activates glial cells which chronically damage neurons
    • hyperinflammatory and hypercoagulable states
      • lead to an increased risk of thrombotic events
    • blood-brain barrier damage and dysregulation
      • results in pathological permeability, allowing blood derived substances and leukocytes to infiltrate the brain parenchyma
    • chronic inflammation in the brainstem may cause autonomic dysfunction
    • effects of long covid in the brain can lead to cognitive impairment
  • (4) possible mechanisms causing post-covid-19 fatigue
    • a range of central, peripheral, and psychological factors may cause chronic fatigue in long covid
      • chronic inflammation in the brain, as well as at the neuromuscular junctions, may result in long term fatigue
      • skeletal muscle
        • sarcolemma damage and fiber atrophy and damage may play a role in fatigue
      • psychological and social factors may play a role in chronic fatigue in long covid

The PHOSP-COVID Collaborative Group undertook a study investigating recovery 1 year after hospital discharge for COVID-19 (4)

  • study (n=2320) reported 29% full recovery at 1 year with female sex, obesity and ventilation associated with being less likely to feel fully recovered at 1 year
    • several inflammatory mediators were increased in individuals with the most severe physical, mental health, and cognitive impairments compared with individuals with milder ongoing impairments

Metformin and risk of long COVID

  • study evidence showed that there was a 42% relative decrease and 4.3% absolute decrease in the Long Covid incidence occurred in participants who received early outpatient COVID-19 treatment with metformin compared to exact-matching placebo (5)

Reference:


Create an account to add page annotations

Annotations allow you to add information to this page that would be handy to have on hand during a consultation. E.g. a website or number. This information will always show when you visit this page.

The content herein is provided for informational purposes and does not replace the need to apply professional clinical judgement when diagnosing or treating any medical condition. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions.

Connect

Copyright 2024 Oxbridge Solutions Limited, a subsidiary of OmniaMed Communications Limited. All rights reserved. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions receives funding from advertising but maintains editorial independence.