This document provides an overview of the diagnosis and management of the 2019 novel coronavirus. It begins with background on coronaviruses in general and then focuses on the 2019-nCoV. It describes the clinical presentation of the infection, from uncomplicated illness to severe pneumonia, acute respiratory distress syndrome, and sepsis. It discusses diagnostic tests and recommendations for supportive care, oxygen therapy, fluid management, antimicrobial use, and monitoring for clinical deterioration. Guidelines are provided for management of hypoxemic respiratory failure, ARDS, septic shock, mechanical ventilation strategies, and ICU complications prevention. Currently no specific anti-coronavirus treatments exist but several clinical trials are underway to evaluate potential antiviral drugs.

1. Diagnosis and Management of 2019
Novel Coronavirus-Infection
Dr. Ahmad Shaddad M.D
Lecturer in Chest Diseases and tuberculosis Department
Faculty of Medicine – Assuit University

2. Contents
 Overview
 Definitions
 Clinical presentation
 Investigations
 Management

3. Overview

4.  Discovered in the 1960s.
 The earliest ones discovered were infectious bronchitis
virus in chickens and two viruses from the nasal cavities of
human patients with the common cold that were
subsequently named human corona virus 229E and human
corona virus OC43.
 Other members of this family are SARS-CoV in
2003, HCoV NL63 in 2004, HKU1 in 2005, MERS-
CoV in 2012, and 2019-nCoV in 2019; most of these have
been involved in serious respiratory tract infections.

5.  "coronavirus" is derived from the Latin corona and the
Greek κορώνη (korṓnē, "garland, wreath"), meaning crown or halo.
 A coronavirus is a kind of common virus that causes an infection in
your nose, sinuses, or upper throat. most corona viruses are not
dangerous.
 Most CoV spread the same way other cold-causing viruses do:
through infected people coughing and sneezing, by touching an
infected person's hands or face, or by touching things such as
doorknobs that infected people have touched.
 Coronaviruses can cause multiple system infections in various
animals and mainly respiratory tract infections in humans, such as
severe acute respiratory syndrome (SARS) and Middle East
respiratory syndrome (MERS).
 At present, information regarding the epidemiology and clinical
features of pneumonia caused by 2019-nCoV is scarce.

6. Corona viruses are named for the crown-like spikes on their
surface. There are four main sub-groupings of corona viruses,
known as alpha, beta, gamma, and delta.
Common human corona viruses
I. 229E (alpha corona virus)
II. NL63 (alpha corona virus)
III. OC43 (beta corona virus)
IV. HKU1 (beta corona virus)
Other human corona viruses
I- MERS-CoV (the beta corona virus that causes
Middle East Respiratory Syndrome, or MERS)
II- SARS-CoV (the beta corona virus that causes
severe acute respiratory syndrome, or SARS)
III- 2019 Novel Coronavirus (2019-nCoV)

7. https://www.cdc.gov/coronavirus/2019-
ncov/index.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcorona
virus%2Fnovel-coronavirus-2019.html
https://www.cdc.gov/sars/index.html
https://www.cdc.gov/coronavirus/mers/index.html

8. Epidemiology
 Novel Coronavirus (2019-nCoV) is a virus identified as the cause
of an outbreak of respiratory illness first detected in Wuhan,
China.
 Early on, many of the patients in the outbreak in Wuhan, China
reportedly had some link to a large seafood and animal market,
suggesting animal-to person spread.
 However, a growing number of patients reportedly have not had
exposure to animal markets, indicating person-to-person spread
is occurring. At this time, it’s unclear how easily or sustainably
this virus is spreading between people.

9. Mode of transmission
 Suspected animal reservoir: seafood and animal market.
 Suspected person-to-person spread
By
1- Droplet infection
2- Air-borne transmission
3- Contact to contaminated surfaces
4- Close contact of confirmed case or dealing with patients’ saliva
secretion and serum.

10. Incubation Period
 The incubation period is the time between infection and the onset of
clinical symptoms of disease.
 Current estimates of the incubation period range from 1-12.5 days with
median estimates of 5-6 days.
 These estimates will be refined as more data become available.
 Based on information from other coronavirus diseases, such as MERS
and SARS, the incubation period of 2019-nCoV could be up to 14 days
and WHO recommends that the follow-up of contacts of confirmed
cases is 14 days.

11. Risk factors
From the data collected by the CDC, the persons at risk are
 Elderly persons above the age of 50 persons with underlying diseases
like diabetes, Parkinson’s disease, cardiovascular diseases.
 Demographically, it can also be stated that the persons living in China
around Wahun town are most at risk, especially those working and
shopping from Animal markets within the localities; and persons
traveling into and out of Wahun.
 Hospital-acquired infection- Health care workers caring for patients
with the 2019-nCoV

12. Pathogenesis of nCoV

13. Current Situation

15. Definitions

16. Patient Under Investigation

17. Confirmed Case
Confirmed isolation of the virus , positive PCR
or positive serological test.

18. Clinical presentation

23. Clinical syndromes associated
with nCoV

24. Uncomplicated illness
Patients with uncomplicated upper respiratory tract viral
infection, may have non-specific symptoms such as fever, cough,
sore throat, nasal congestion, malaise, headache, muscle pain or
malaise. The elderly and immunosuppressed may present with
atypical symptoms. These patients do not have any signs of
dehydration, sepsis or shortness of breath.

25. Mild pneumonia
 Patient with pneumonia and no signs of severe pneumonia.
 Child with non-severe pneumonia has cough and no difficulty
breathing.

26. Severe pneumonia
 Adolescent or adult: fever or suspected respiratory infection, plus one of
 respiratory rate >30 breaths/min,
 severe respiratory distress, or
 SpO2 <90% on room air .
 Child with cough or difficulty in breathing, plus at least one of the
following:
 central cyanosis or
 SpO2 <90%;
 severe respiratory distress (e.g. grunting, very severe chest indrawing)
 signs of pneumonia with a general danger sign: inability to breastfeed or
drink, lethargy or unconsciousness, or convulsions.

27. Acute Respiratory Distress Syndrome
Onset: new or worsening respiratory symptoms within one week of known clinical insult.
Chest imaging (radiograph, CT scan, or lung ultrasound): bilateral opacities, not fully explained by effusions, lobar or lung
collapse, or nodules.
Origin of oedema: respiratory failure not fully explained by cardiac failure or fluid overload. Need objective assessment (e.g.
echocardiography) to exclude hydrostatic cause of oedema if no risk factor present.
Oxygenation (adults):
• Mild ARDS: 200 mmHg < PaO2/FiO2 ≤ 300 mmHg (with PEEP or CPAP ≥5 cmH2O,7 or non-ventilated 8)
• Moderate ARDS: 100 mmHg < PaO2/FiO2 ≤200 mmHg with PEEP ≥5 cmH2O,7 or non-ventilated 8)
• Severe ARDS: PaO2/FiO2 ≤ 100 mmHg with PEEP ≥5 cmH2O,7 or non-ventilated 8)
• When PaO2 is not available, SpO2/FiO2 ≤315 suggests ARDS (including in non-ventilated patients)
Oxygenation (children; note OI = Oxygenation Index and OSI = Oxygenation Index using SpO2):
• Bilevel NIV or CPAP ≥5 cmH2O via full face mask: PaO2/FiO2 ≤ 300 mmHg or SpO2/FiO2 ≤264
• Mild ARDS (invasively ventilated): 4 ≤ OI < 8 or 5 ≤ OSI < 7.5
• Moderate ARDS (invasively ventilated): 8 ≤ OI < 16 or 7.5 ≤ OSI < 12.3
• Severe ARDS (invasively ventilated): OI ≥ 16 or OSI ≥ 12.3

28. Sepsis
 Life-threatening organ dysfunction caused by a
dysregulated host response to suspected or proven
infection, with organ dysfunction.
 Signs of organ dysfunction include: altered mental
status, difficult or fast breathing, low oxygen
saturation, reduced urine output, fast heart rate, weak
pulse, cold extremities or low blood pressure, skin
mottling, or laboratory evidence of coagulopathy,
thrombocytopenia, acidosis, high lactate or
hyperbilirubinemia.

29. Septic Shock
 Adults: persisting hypotension despite volume resuscitation, requiring
vasopressors to maintain MAP ≥65 mmHg and serum lactate level >2
mmol/L.
 Children (based on [12]): any hypotension (SBP <5th centile or >2 SD
below normal for age) or 2-3 of the following: altered mental state;
tachycardia or bradycardia (HR <90 bpm or >160 bpm in infants and
HR <70 bpm or >150 bpm in children); prolonged capillary refill (>2
sec) or warm vasodilation with bounding pulses; tachypnea; mottled
skin or petechial or purpuric rash; increased lactate; oliguria;
hyperthermia or hypothermia.

30. Investigations

32. Definitive diagnostic tests

36. Management

37. Immediate implementation of
appropriate infection prevention control
(IPC) measures

39. Early supportive therapy and
monitoring

40.  Give supplemental oxygen therapy immediately to patients with
SARI and respiratory distress, hypoxaemia, or shock.
 Initiate oxygen therapy at 5 L/min and titrate flow rates to reach target
SpO2 ≥90% in non-pregnant adults and SpO2 ≥92-95 % in pregnant
patients.
 Children with emergency signs (obstructed or absent breathing, severe
respiratory distress, central cyanosis, shock, coma or convulsions)
should receive oxygen therapy during resuscitation to target SpO2
≥94%; otherwise, the target SpO2 is ≥90%.

41.  Use conservative fluid management in patients with SARI
when there is no evidence of shock.
Patients with SARI should be treated cautiously with intravenous
fluids, because aggressive fluid resuscitation may worsen
oxygenation, especially in settings where there is limited
availability of mechanical ventilation.
 Give empiric antimicrobials to treat all likely pathogens
causing SARI. Give antimicrobials within one hour of
initial patient assessment for patients with sepsis.

42.  Do not routinely give systemic corticosteroids for treatment
of viral pneumonia or ARDS outside of clinical trials unless
they are indicated for another reason.
 Closely monitor patients with SARI for signs of clinical
deterioration, such as rapidly progressive respiratory
failure and sepsis, and apply supportive care interventions
immediately.
 Understand the patient’s co-morbid condition(s) to tailor
the management of critical illness and appreciate the
prognosis.

43. Management of hypoxemic
respiratory failure and ARDS

44.  Recognize severe hypoxemic respiratory failure when a
patient with respiratory distress is failing standard oxygen
therapy.
 Patients may continue to have increased work of breathing or
hypoxemia even when oxygen is delivered via a face mask
with reservoir bag (flow rates of 10-15 L/min, which is
typically the minimum flow required to maintain bag inflation;
FiO2 0.60-0.95).
 Hypoxemic respiratory failure in ARDS commonly results
from intrapulmonary ventilation-perfusion mismatch or shunt
and usually requires mechanical ventilation.

45.  High-flow nasal oxygen (HFNO) or non-invasive
ventilation (NIV)
Should only be used in selected patients with hypoxemic
respiratory failure. The risk of treatment failure is high and
patients treated with either HFNO or NIV should be closely
monitored for clinical deterioration.

46. Mechanical ventilation strategies

47.  Endotracheal intubation should be performed by a trained and experienced
provider using airborne precautions.
 Implement mechanical ventilation using lower tidal volumes (4–8 ml/kg predicted
body weight, PBW) and lower inspiratory pressures (plateau pressure <30 cmH2O).
 patients with severe ARDS, prone ventilation for >12 hours per day is
recommended.
 In patients with moderate or severe ARDS, higher PEEP instead of lower PEEP is
suggested.
 In patients with moderate-severe ARDS (PaO2/FiO2 <150), neuromuscular
blockade by continuous infusion should not be routinely used.
 In settings with access to expertise in extracorporeal life support (ECLS),
consider referral of patients with refractory hypoxemia despite lung protective
ventilation.

48. Management of septic shock

49.  In resuscitation from septic shock in adults, give at least 30
ml/kg of isotonic crystalloid in adults in the first 3 hours.
 Do not use hypotonic crystalloids, starches, or gelatins for
resuscitation.
 Administer vasopressors when shock persists during or after
fluid resuscitation. The initial blood pressure target is MAP
≥65 mmHg.
 If signs of poor perfusion and cardiac dysfunction persist
despite achieving MAP target with fluids and vasopressors,
consider an inotrope such as Dobutamine.

50. Prevention of complications in ICU

52. Specific anti-Novel-CoV treatments and clinical
research

53.  So far no specific medicine and no vaccine has been made for corona
virus.
 A randomized, controlled trial of antiviral drug Remdesivir is currently
underway in China in hopes that it will be an effective treatment for the
2019 Novel Coronavirus (2019-nCoV).
 Another Randomised controlled trial has been initiated quickly to
assess the efficacy and safety of combined use of lopinavir and
Ritonavir in patients hospitalised with 2019- nCoV infection.
 Third study was to evaluated the antiviral efficiency of five FAD-
approved drugs including ribavirin, penciclovir, nitazoxanide,
nafamostat, chloroquine and two well-known broad-spectrum
antiviral drugs remdesivir (GS-5734) and favipiravir (T-705) against a
clinical isolate of 2019-nCoV in vitro.

54. Prevention is the best available
option at the current time