COVID 19: Key information for clinicians

Within the Trust intranet there is a prominent COVID section which is updated daily. Below is key information for clinicians.


The majority of infections either do not produce any symptoms or cause a mild flu-like illness that resolves spontaneously.

Common clinical presentations of COVID-19 are fever, dry cough, new onset anosmia, dyspnoea, anorexia, myalgia, headache, unexplained gastrointestinal symptoms and fatigue. Runny noses and productive cough are uncommon, except in children.

Fever is present in 99%, fatigue in 70%, dry cough in 59%, anorexia in 40%, myalgia in 35%, Dyspnoea in 31%.

In Chinese studies dyspnoea developed after a median of five days after the onset of symptoms, and hospital admission occurred after a median of seven days of symptoms. In another study, the median time to dyspnoea was eight days.

The median duration between onset of symptoms and ICU admission has been 9 to 10 days.

Incubation period, susceptibility, severity and recovery

The incubation is 1 to 14 days (usually 3 to 7 days), transmission can also occur during incubation.

Pregnant women, the new born and the elderly, and patients with comorbidities (e.g. diabetes mellitus, hypertension, cardiovascular, chronic lung and chronic kidney disease) are particularly susceptible to COVID-19 infection and are likely to have more severe illness.

About 16-20% cases have been classified as ‘severe’ or ‘critical’

According to the WHO, recovery time appears to be around two weeks for mild infections and three to six weeks for severe disease.







Low in 80% of cases


Normal / High


Usually mildly low

<100 poor prognosis



1 poor prognosis



125 poor prognosis. If normal consider alternate diagnosis e.g. heart failure


Mildly High

Caution: no shock

Urea / Creat

Mildly High

AKI usually mild



Rhabdomyolysis may contribute to AKI



5 times normal, transient, no fulminant hepatitis, rise day 14

Chest X-Ray findings typically show patchy ground glass opacities which may be unilateral (25%), peripheral and basal. The number of lung segments increases with more severe disease. Over time, patches coalesce into more dense consolidation. Changes may be subtle, or X-rays may appear normal (40%). Effusions, cavitation, masses and lymphadenopathy are rare (5%).

Chest CT may be helpful where doubt in diagnosis exists.


Fluids: Avoid fluid overload but equally avoid volume depletion, AKI is a clear risk. BP usually normal – Consider Pressors / Inotropes if not hypovolaemic

Antibiotics: 16% secondary infection, consider 48 hours then stop if culture negative.

Antivirals / HIV meds: Studies ongoing (Trust guide)

Steroids: No evidence of benefit, may be harmful, increase viral shedding but consider for other indications e.g. asthma, refractory septic shock.

High flow Oxygen therapy (Optiflow): remember this is an aerosol generating procedure but 1/10th the velocity of a cough (40-60 L/min vs cough 400 L/min). Consider using 15-30 L/min (ie close to RR of sick patient). If required FIO2 > 75 % = likely to need intubation

Rapid deterioration from NIV to needing intubation – consider early intubation instead Intubation: remember this is an AGP

Thromboprophylaxis routinely unless contraindication, bleeding or PT / APTT >2ULN, Platelet count <30, fibrinogen <1g/L. Discuss these patients with haematology. Remember Chinese experience was that LMWH thromboprophylaxis was associated with significantly better survival in disease with raised D-dimer and clotting abnormalities.


From Chinese data the disease was Mild (no or mild pneumonia) in 81%; Severe disease (e.g., with dyspnoea, hypoxia, or >50% lung involvement on imaging within 24 to 48 hours) was reported in 14%; Critical disease (e.g., with respiratory failure, shock, or multiorgan dysfunction) was reported in 5%. Italian ICU data indicates 26% mortality. The overall world case fatality rate is 6.0% and our UK mortality rate in known cases is 12.3%.