2. Interactive Case Presentation
Gamal Rabie Agmy ,MD ,FCCP
Professor of Chest Diseases, Assiut University

3. A 36-year-old female presented
with a 3-day history of increasing
shortness of breath, cough with
yellowish sputum, haemoptysis,
pleuretic chest pain, nausea,
vomiting and rigors.

4. The patient was an intravenous
drug user (IVDU) who smoked 20
cigarettes per day and denied
drinking alcohol. Her only past
medical history was of mild
asthma, for which salbutamol
was taken as needed.

5. The patient appeared distressed
and unwell. Her temperature was
39.3°C, and she was tachycardic (120
beats per minute), hypotensive (BP
85/55 mHg) and hypoxic
(O2
saturation 82% on air with a
respiratory rate of 32 breaths per
minute).

6. *There were needle marks in both groins and
forearms.
*Heart sounds were normal with no murmurs.
*Chest examination demonstrated scattered
crepitations all over the chest
*Abdominal and neurological examinations
were unremarkable

7. Initial investigations were as follows:
white
blood
cells
13.2×109·L-1,
neutrophils 9.7×109·L-1, haemoglobin 11.3
g·dL-1, platelets 71×109·L-1, INR of 1.5,
creatinine 2.3mg/DL, urea 84 mg/DL,
alkaline phosphatase 195 IU·L-1, alanine
aminotransferase 63 IU·L-1, and Creactive protein 285 mg·L-1.

8. Initial
Arterial
blood
gases
on
air showed : pH 7.60, partial pressure of O2 50
mmHg, partial pressure of CO2 28 mmHg and
bicarbonate 24 mLeq/L.

9. Depending on clinical picture and
investigations; what is your diagnosis
1-Pulmonary TB
2-Nosocomial pneumonia.
3- severe Pneumonia in immunocompromised
host
4-Simple Pneumonia in immunocompromised
host

10. Depending on clinical picture and
investigations; what is your diagnosis
1-Pulmonary TB
2-Nosocomial pneumonia.
3- severe Pneumonia in immunocompromised
host
4-Simple Pneumonia in immunocompromised
host

11. Can you Interpret the arterial blood gases
(PH 7.60, Pa O2 50 mmHg, Pa CO2 28 mmHg and
bicarbonate 24 mLeq/L )
1- Acute type 1 respiratory failure
2- Acute on top of chronic type 1 respiratory
failure
3- Chronic type 1 respiratory failure
4- Type 11 respiratory failure

12. Can you Interpret the arterial blood gases
(PH 7.60, Pa O2 50 mmHg, Pa CO2 28 mmHg and
bicarbonate 24 mLeq/L )
1- Acute type 1 respiratory failure
2- Acute on top of chronic type 1 respiratory
failure
3- Chronic type 1 respiratory failure
4- Type 11 respiratory failure

13. The patient was initially treated for severe
pneumonia and a chest radiography
followed by computed (CT) scan of the chest
were obtained .

15. On the basis of radiological
findings, what is your diagnosis
1-Septic pulmonary embolism.
2- Cavitating pneumonia.
3- Pulmonary TB
4-Cavitating secondaries

16. On the basis of radiological
findings, what is your diagnosis
1-Septic pulmonary embolism.
2- Cavitating pneumonia.
3- Pulmonary TB
4-Cavitating secondaries

17. What is best next investigations
1-Sputum culture sensitivity.
2-Blood culture.
3-TTE
4- 2&3
5-All of above

18. What is best next investigations
1-Sputum culture sensitivity.
2-Blood culture.
3-TTE
4- 2&3
5-All of above

19. In acute bacterial endocarditis ,
TTE can be negative
1- Yes
2- No

20. In acute bacterial endocarditis ,
TTE can be negative
1- Yes
2- No

21. *On TTE, vegetations<4 mm in
diameter may not be seen.
*The sensitivity of TTE compared
with TOE is 40–63% versus 90–
100%.

22. In septic pulmonary embolism ,
what is the commonest organism
demonstrated by blood culture
1- Streptococci
2- Gram negative bacteria
3- Staphylococcus aureus
4- Anaerobes

23. In septic pulmonary embolism ,
what is the commonest organism
demonstrated by blood culture
1- Streptococci
2- Gram negative bacteria
3- Staphylococcus aureus
4- Anaerobes

24. S. aureus is the main agent,
followed by various streptococci,
aerobic
Gram-negative
rods,
anaerobic cocci and bacilli

25. On the basis of the CT findings, the
diagnosis of infected pulmonary emboli was
considered
and
right-sided
infective
endocarditis (IE) was suspected. This was
supported by positive blood culture result.
However, the transthoracic echocardiogram
(TTE) showed no vegetations.

26. Despite treatment with
appropriate highdose
intravenous antibiotics, the
patient deteriorated
progressively,
becoming
confused and agitated. She
remained
febrile,
hypotensive and hypoxic.
Approximately, 72 hours
post
admission,
she
developed a rash

27. The patient's level of consciousness continued to
deteriorate such that the airway could no longer be
protected. Subsequently, she was transferred to the
intensive care unit (ICU) where she was sedated and
intubated. Inotropic support was required.

28. For the next 10 days, despite appropriate
antibiotic and supportive therapy, the
patient failed to improve. She developed
spontaneous
pneumothoraces
and
several other complications, including
anaemia, profound hypoalbuminaemia
(albumin 9 g·L-1), massive oedema of all
limbs and severe lower limb ulceration.

29. Improvement then began
gradually over the next 7
days. She required less
ventilatory support and
was weaned off inotropes.
However, she remained
unresponsive
despite
cessation of all
sedation; hence, a CT
scan of the brain was
obtained .

30. Suggest possible mechanisms that could
explain systemic embolisation in right-sided IE.
1. Concurrent involvement of both left and right
ventricles.
2. Paradoxical embolism.
3. Acquired pulmonary arteriovenous malformation.
4. Metastatic as part of generalised septicaemia.
5-All of above

31. Suggest possible mechanisms that could
explain systemic embolisation in right-sided IE.
1. Concurrent involvement of both left and right
ventricles.
2. Paradoxical embolism.
3. Acquired pulmonary arteriovenous malformation.
4. Metastatic as part of generalised septicaemia.
5-All of above

32. Over the course of several weeks,
the patient gradually regained
consciousness, intelligent speech,
and motor function on the left side.

33. After 8 weeks in hospital, she was
transferred to a rehabilitation
facility. On discharge from this
facility,
she
was
able
to
communicate intelligently, mobilise
without assistance and was fully
independent.

34. The main pathophysiologic mechanism
of RF in pulmonary embolism is :
•
•
•
•
1-Shunt
2-Dead space ventilation
3-Hypoventilation
4-Diffusion defect

35. The main pathophysiologic mechanism
of RF in pulmonary embolism is :
•
•
•
•
1-Shunt
2-Dead space ventilation
3-Hypoventilation
4-Diffusion defect

36. Optimal V/Q matching

37. Dead Space

38. Shunt

39. Learning points
1. Endocarditis is common in IVDUs and
can
cause
catastrophic
septic
embolisation.
2. Endocarditis may be difficult to be
clearly diagnosed.
3-Endocarditis can be diagnosed in
negative TTE

40. Learning points
4. Antibiotics use should cover S. aureus in
septic patients known to abuse intravenous
drugs, but positive microbiology must be
sought as polymicrobial and fungal infections
are common.
5-The main pathophysiologic of respiratory
failure in PE is dead space ventilation
6. Patients can make a full recovery despite
overwhelming
sepsis
and
neurological
damage, and should be treated aggressively.