Interactive case presentation

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Information about Interactive case presentation
Health & Medicine

Published on February 21, 2014

Author: GamalAgmy

Source: slideshare.net

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

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.

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.

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).

*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 Creactive 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. 3- severe Pneumonia in immunocompromised 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 ) 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

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 1-Septic pulmonary 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 4- 2&3 5-All of above

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

In acute bacterial endocarditis , TTE can be negative 1- Yes 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 3- Staphylococcus aureus 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 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

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.

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.

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 .

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

Dead Space

Shunt

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. 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.

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