Assiut Interactive Case

Presentation

Moderator:

Professor Gamal Agmy

Panelists:

1-Dr Samiaa Hamdy

2-Dr Mohamed Barkat

3-Dr Ahmed Metwally

4-Dr Hassen Byomy

5-Dr Manal Ahmed

A 36-year-old male presented with a

3-day history of increasing

shortness of breath, cough with

yellowish sputum, haemoptysis,

pleuretic chest pain, nausea,

vomiting and rigors.

The patient was an intravenous

drug user (IVDU) who smoked 20

cigarettes per day and denied

drinking alcohol. His only past

medical history was of mild

asthma, for which salbutamol was

taken as needed.

The patient appeared distressed

and unwell. His temperature was

39.3°C, and he 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).

*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

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 C-reactive protein 285 mg·L-1.

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.

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

Depending on clinical picture and

investigations; what is your diagnosis?

1-Pulmonary TB

2-Nosocomial pneumonia.

immunocompromisedsevere Pneumonia in -3

host

4-Simple Pneumonia in immunocompromised

host

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

Can you Interpret the arterial blood gases

(PH 7.60, Pa O2 50 mmHg, Pa CO2 28

mmHg and bicarbonate 24 mLeq/L ) ?

respiratory failure1 Acute type -1

2- Acute on top of chronic type 1 respiratory

failure

3- Chronic type 1 respiratory failure

4- Type 11 respiratory failure

The patient was initially treated for

severe pneumonia and a chest

radiography followed by computed

(CT) scan of the chest were obtained .

On the basis of radiological findings, what

is your diagnosis ?

1-Septic pulmonary

embolism.

2- Cavitating pneumonia.

3- Pulmonary TB

4-Cavitating secondaries

On the basis of radiological findings, what

is your diagnosis ?

Septic pulmonary -1

embolism.

2- Cavitating pneumonia.

3- Pulmonary TB

4-Cavitating secondaries

What is best next investigations ?

1-Sputum culture sensitivity.

2-Blood culture.

3-TTE

4- 2&3

5-All of above

What is best next investigations ?

1-Sputum culture sensitivity.

2-Blood culture.

3-TTE

3 &2 -4

5-All of above

In acute bacterial endocarditis , TTE can be

negative?

1- Yes

2- No

In acute bacterial endocarditis , TTE can be

negative?

Yes -1

2- No

*On TTE, vegetations<4 mm in diameter

may not be seen.

*The sensitivity of TTE compared with TOE

is 40–63% versus 90–100%.

In septic pulmonary embolism , what is the

commonest organism demonstrated by

blood culture ?

1- Streptococci

2- Gram negative bacteria

3- Staphylococcus aureus

4- Anaerobes

In septic pulmonary embolism , what is the

commonest organism demonstrated by

blood culture ?

1- Streptococci

2- Gram negative bacteria

aureusStaphylococcus -3

4- Anaerobes

S. aureus is the main agent, followed

by various streptococci, aerobic

Gram-negative rods, anaerobic cocci

and bacilli .

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.

Despite treatment with

appropriate high dose IV

antibiotics, the patient

deteriorated progressively

, becoming confused and

agitated. He remained

febrile, hypotensive and

hypoxic. Approximately,

72 hours post admission,

he developed a rash

The patient's level of consciousness

continued to deteriorate such that the

airway could no longer be protected.

Subsequently, he was transferred to

the intensive care unit (ICU) where he

was sedated and intubated. Inotropic

support was required.

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

0.9 g·L-1), massive oedema of all limbs

and severe lower limb ulceration.

Improvement then

began gradually over the

next 7 days. He required

less ventilatory support

and was weaned off

inotropes. However, he

remained unresponsive

despite cessation of all

sedation; hence, a CT

scan of the brain was

obtained .

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

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

Over the course of several weeks,

the patient gradually regained

consciousness, intelligent speech,

and motor function on the left

side.

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.

The main pathophysiologic mechanism of

RF in pulmonary embolism is :

•1-Shunt

•2-Dead space ventilation

•3-Hypoventilation

•4-Diffusion defect

The main pathophysiologic mechanism of

RF in pulmonary embolism is :

•1-Shunt

•2-Dead space ventilation

•3-Hypoventilation

•4-Diffusion defect

Optimal V/Q matching

Shunt

Optimal V/Q matching

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

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.

Learning points

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.