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COVID 19 – What we know
so far
Dr Joy Halliday
Consultant Intensive Care
Pathophysiology
 ARDS
 Diffuse alveolar damage – direct virus damage rather than pure hyperinflammation
 Pneumocytes with viral cytopathic effect are seen
 Cytokine storm
 Some patients react with an exuberant cytokine storm
 increased CRP and ferritin levels
 These appear track disease severity and mortality
Stages of Illness
 1) Replicative stage
 viral replication occurs over several days
 relatively mild symptoms occur due to direct viral cytopathic effect and innate immune
responses
 2) Adaptive immunity stage
 leads to falling viral titres however:
 Increase in levels of inflammatory cytokines leading to tissue damage and clinical
deterioration
This progression may explain why patients are relatively well for a few days and then
suddenly deteriorate when they enter the adaptive immunity stage
Signs and Symptoms
Signs and Symptoms
 Fever
 Variable (present 43-98%)
 Absence of fever does not exclude COVID 19
 GI upset
 Up to 10% initially present with nausea or diarrhoea
 Silent Hypoxaemia
 Respiratory failure without dyspnoea is common especially in the elderly
Typical disease course
Laboratory Picture
Laboratory findings
 White Blood count
 WBC tends to be normal
 Lymphopenia in 80% patients
 Mild thrombocytopenia common
 Inflammatory markers
 CRP increased and seems to track disease severity and prognosis
Sensitivity of investigations
 PCR seems to have a sensitivity of around 75%
 A single negative RT-PCR does not exclude COVID 19 (especially when obtained
from a NP source or taken relatively early in the disease course)
 If RT-PCR is negative but suspicion is high then ongoing isolation abd re-sampling
several days later should be considered
CXR
Patchy ground glass opacities
predominantly peripheral and basal
Over time, ground glass opacities coalesce
into more dense consolidation
Infiltrates may initially be subtle on CXR
Pleural effusions, cavities and
lymphadenopathy uncommon and should
herald investigations for other diagnoses
CT chest
CT scanning will show anything from
minor infiltrates to multi-lobar
ground glass opacities and
consolidation
Sensitivity of a ‘positive scan’ is
about 86-97% but is less sensitive
with constitutional symptoms only
Treatment and Management
 Largely supportive
 Anti-viral therapy
 Remdesivir, Lopinavir/ritonavir – protease inhibitors that block viral replication
 Were used in MERS-CoV
 Chloroquine
 Anti-viral activity as well as immunosuppressive
 ? Favourable results in China – mixed messages
 Steroids
 Not generally used. May increase viral shedding
Treatment and Management
 Avoid Fluid resuscitation
– cause of death is nearly always ARDS and not shock
 Haemodynamic Support
 Elevated Troponin correlates mortality – about 7% get fulimant myocarditis
 Invasive Mechanical Ventilation
 Open lung strategy
 4-6ml/kg TV
 Patients require PEEP and respond well to proning
 Permissive hypercapnia
 Ecmo
Prognosis
 Lots of people with mild illness who don’t present or get accounted for so remains
unclear
 Among hospitalised patients
 10-20% are admitted to ICU
 3-10% require intubation
 2-5% die
Epidemiological and laboratory risk factors
 Older age
 Male sex
 Medical co-morbidities
 COPD
 Hypertension and CAD
 Diabetes
 Lymphopenia/high CRP/high troponin
Any questions?

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COVID-19 Pathophysiology, Signs, Treatment

  • 1. COVID 19 – What we know so far Dr Joy Halliday Consultant Intensive Care
  • 2. Pathophysiology  ARDS  Diffuse alveolar damage – direct virus damage rather than pure hyperinflammation  Pneumocytes with viral cytopathic effect are seen  Cytokine storm  Some patients react with an exuberant cytokine storm  increased CRP and ferritin levels  These appear track disease severity and mortality
  • 3. Stages of Illness  1) Replicative stage  viral replication occurs over several days  relatively mild symptoms occur due to direct viral cytopathic effect and innate immune responses  2) Adaptive immunity stage  leads to falling viral titres however:  Increase in levels of inflammatory cytokines leading to tissue damage and clinical deterioration This progression may explain why patients are relatively well for a few days and then suddenly deteriorate when they enter the adaptive immunity stage
  • 5. Signs and Symptoms  Fever  Variable (present 43-98%)  Absence of fever does not exclude COVID 19  GI upset  Up to 10% initially present with nausea or diarrhoea  Silent Hypoxaemia  Respiratory failure without dyspnoea is common especially in the elderly
  • 8. Laboratory findings  White Blood count  WBC tends to be normal  Lymphopenia in 80% patients  Mild thrombocytopenia common  Inflammatory markers  CRP increased and seems to track disease severity and prognosis
  • 9. Sensitivity of investigations  PCR seems to have a sensitivity of around 75%  A single negative RT-PCR does not exclude COVID 19 (especially when obtained from a NP source or taken relatively early in the disease course)  If RT-PCR is negative but suspicion is high then ongoing isolation abd re-sampling several days later should be considered
  • 10. CXR Patchy ground glass opacities predominantly peripheral and basal Over time, ground glass opacities coalesce into more dense consolidation Infiltrates may initially be subtle on CXR Pleural effusions, cavities and lymphadenopathy uncommon and should herald investigations for other diagnoses
  • 11. CT chest CT scanning will show anything from minor infiltrates to multi-lobar ground glass opacities and consolidation Sensitivity of a ‘positive scan’ is about 86-97% but is less sensitive with constitutional symptoms only
  • 12. Treatment and Management  Largely supportive  Anti-viral therapy  Remdesivir, Lopinavir/ritonavir – protease inhibitors that block viral replication  Were used in MERS-CoV  Chloroquine  Anti-viral activity as well as immunosuppressive  ? Favourable results in China – mixed messages  Steroids  Not generally used. May increase viral shedding
  • 13. Treatment and Management  Avoid Fluid resuscitation – cause of death is nearly always ARDS and not shock  Haemodynamic Support  Elevated Troponin correlates mortality – about 7% get fulimant myocarditis  Invasive Mechanical Ventilation  Open lung strategy  4-6ml/kg TV  Patients require PEEP and respond well to proning  Permissive hypercapnia  Ecmo
  • 14. Prognosis  Lots of people with mild illness who don’t present or get accounted for so remains unclear  Among hospitalised patients  10-20% are admitted to ICU  3-10% require intubation  2-5% die
  • 15. Epidemiological and laboratory risk factors  Older age  Male sex  Medical co-morbidities  COPD  Hypertension and CAD  Diabetes  Lymphopenia/high CRP/high troponin