ICU and pulmonary medicine

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Today lecture

Many thanks for Dr Ahmad Adel

as when there is secondary infection or invasion of the chest wall.
Antibody detection (usually enzyme-linked immunosorbent assay) is more sensitive than antigen detection for diagnosis of E granulosus. In this case, the patient underwent surgical resection, which is the treatment of choice for complicated pulmonary CEs. The histopathology from the surgical specimen shows the host tissue encapsulating the cyst wall, which is composed of an acellular laminated layer and a nucleate germinal layer from which the brood capsule arises (Figure 7). Medical management is a useful adjunctive therapy to surgery.
Albendazole is the primary antiparasitic agent used for treatment of pulmonary CE. Pyrimethamine and sulfadiazine is an effective antibiotic regimen for toxoplasmosis, which is not present in this case (choice A is incorrect). Toxoplasma pneumonia should be considered in the differential diagnosis of a respiratory illness with bilateral infiltrates on chest imaging, especially in immunocompromised hosts. Praziquantel is the treatment of choice for paragonimiasis (choice C is incorrect).
Recurrent hemoptysis is the most common symptom of late infection due to paragonimiasis, with common radiologic findings including pleural effusion, hydropneumothorax, pulmonary nodules, airspace consolidation, and cysts. Ivermectin is commonly used for the treatment of strongyloidiasis (choice D is incorrect).
Pulmonary manifestations of strongyloidiasis are protean and can present as pulmonary infiltrates with eosinophilia, asthma without infiltrates, hemoptysis due to alveolar hemorrhage, and hyperinfection syndrome.

This patient has severe pulmonary cystic echinococcosis
(CE), a zoonosis caused by the larvae of the dog tapeworm Echinococcus granulosus and therefore should be treated with albendazole (choice B is correct). In adults, cysts occur most frequently in the liver, followed by the lungs. Most symptoms of CE are caused by mass effect from the cyst volume, which exerts pressure on the surrounding tissues. The most common symptoms of pulmonary CE include cough, chest pain, dyspnea, and hemoptysis. When cysts rupture, either by spontaneous trauma or during medical intervention, protoscolices contained in the cystic fluid may disseminate into the tracheobronchial tree or the pleural cavity.
Tracheobronchial involvement can lead to cough, chest pain, or hemoptysis; pleural cavity involvement can result in pneumothorax, pleural effusion, or empyema.
Pulmonary CEs may also lead to a pulmonary eosinophilia, particularly in instances of rupture. This patient also had pulmonary eosinophilia as a result of tracheobronchial rupture as well as a pneumothorax and bronchopleural fistula as a result of pleural rupture of the pulmonary CE. Most often the diagnosis of pulmonary CE can be established with a combination of imaging and serology. An uncomplicated pulmonary CE appears as a well-defined homogeneous radiopacity on a chest radiograph. When it erodes into a bronchus, there is introduction of air between the pericyst and the endocyst appearing as a radiolucent rim around the cyst, as a crescent sign, on plain chest radiography and CT scanning (Figure 6). With further collapse of the endocyst, the membranes floating in the remaining fluid are known as the water lily sign (also known as the Camelot sign). On CT imaging, intact pulmonary CEs can be difficult to differentiate from other pulmonary cysts. CT can be very helpful when there is rupture of the pulmonary CE into the tracheobronchial tree or the pleural cavity, as well as

اجابة السؤال 👇🏼👇🏼👇🏼
B

Histology from the right middle lobectomy is shown
(Figure 5).

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A 28-year-old woman with no significant medical history presents with subacute onset of cough, subjective fevers, and right-sided pleuritic pain. She denies night sweats or weight loss.
On physical examination, she is febrile to 39.0°C, and her heart rate is 133/min, BP is 103/58 mm Hg, respiratory rate is 22/min, and SpO, is 93% on room air. Aside from diffuse end-expiratory wheezing and diminished breath sounds in the right midaxillary region, the remainder of her examination is unremarkable.
Laboratory analysis is notable for a WBC count of 14,700/ ML (14.7 × 10º/L), with 3,000/uL (3 × 10'/L eosinophils on the differential; hematocrit is 38% (0.38); and platelet count is 393 x 10¾L (393 × 10ºL). Total IgE is 4 U/L.
Basic metabolic panel and liver tests are within normal limits. HIV is negative. An extensive infectious workup, including sputa for acid-fast bacilli and Mycobacterium tuberculosis polymerase chain reaction, is negative. A chest radiograph is obtained (Figure 1), followed by a chest CT scan with IV contrast (Figure 2). A bronchoscopy with BAL is performed. BAL cell and differential counts are notable for total nucleated cell count of 559/mm3, with 45% lymphocytes and 45% eosinophils.
The patient is started on corticosteroids, with notable improvement of her symptoms and airspace opacities. She is discharged home, though presents 2 weeks later with acute-onset dyspnea and severe pleuritic chest pain. A chest radiograph obtained at the time is shown (Figure 3).
She undergoes chest tube thoracostomy. Her course is complicated by development of a bronchopleural fistula (Figure 4). She subsequently undergoes right posterolateral thoracotomy with right middle lobectomy with en bloc lower wedge resection and decortication.

💉Causes of neonatal cyanosis:
A- with increased work of breathing :
PULMONARY e.g.
• sever RDS.
• congenital pneumonia.
• meconium aspiration syndrome.
• pneumothorax.
• Diaphragmatic hernia.
• persistent pulmonary hypertension of newborn.
CARDIAC:
• congenital cyanotic heart disease with increase pulmonary blood flow e.g. TGA, VSD.
• congenital heart disease with critical obstruction.
B- With normal work of breathing :
• Cardiac :congenital cyanotic heart disease with decrease pulmonary blood flow.
• Hematologic: polycythemia and met hemoglobin snow.
C- With decreased work of breathing :
• central respiratory failure.

💡Causes of ((Acute respiratory distress)) in pregnancy:

1- preeclampsia/eclampsia .
2- Tocolytic induced pulmonary edema.
3- chorioaminitis.
4- Amniotic fluid embolism .
5- Trophoblastic embolism .
6- placental abruption.
7- Ovarian hyperstimulation syndrome.
8- Endometritis.
9- Septic abortion.
10- Retained products of conception.

Absolute indications of invasive mechanical ventilation in sever acute #Asthma patient :

➔ Coma.
➔ Respiratory or cardiac arrest.
➔ Refractory hypoxemia.

Relative indications :
➔ Inadequate response to initial.
management.
➔ Hypercapnia.
➔ Fatigue.
➔ Cardiovascular compromise.

Indications of invasive Mechanical Ventilation in COPD patient..??

➔ PaO2 < 40 mmhg
➔ Ph < 7.25.
➔ CO2 > 60 mmhg.
➔ Respiratory arrest.
➔ Cardiovascular collapse.
➔ Severe exacerbation with a lot of
secretions.

⛔️⛔️⛔️

When to use O2 therapy in COPD patient ??

➔ Po2 < 55 or  Sat < 88%

#Or

➔ Po2 < 60  sat < 90% with right sided HF.

Many thanks for P Amany Ezz Alarab

بسم الله الرحمن الرحيم
Today lecture

🩺Setting PEEP in the Intubated COPD Patient
by Mike Winters, MD

PEEP in the Ventilated COPD Patient?
Patients with acute respiratory failure secondary to COPD often have dynamic hyperinflation and intrinsic PEEP (PEEPi).
Both dynamic hyperinflation and PEEPi adversely effect pulmonary mechanics, markedly increase the work of breathing, impair respiratory muscle function, and can result in hemodynamic compromise.
It has traditionally been felt that the application of external PEEP in the intubated COPD patient may worsen hyperinflation.
Importantly, external PEEP has been shown to improve ventilator synchrony and decrease the work of breathing.
PEEPi is measured using an end-expiratory hold maneuver in a passive, relaxed patient.
External PEEP can then be set to approximately 70% of PEEPi, followed by frequent monitoring of plateau pressures in a volume-cycled ventilation mode.
References
Jubran A. Setting positive end-expiratory pressure in the severely obstructive patient. Curr Opin Crit Care. 2024; 30:89-96.

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Many thanks for P Sabah Oraby

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اجابة السؤال 👇🏼👇🏼👇🏼
D

While acute mitral regurgitation can cause localized pulmonary edema due to the regurgitant jet interfering with pulmonary venous inflow to the left atrium, this typically occurs in the right upper lobe, which is not the case in this patient (choice A is incorrect.) Allergic reactions to anesthetics may produce bronchospasm or pulmonary edema but should not produce sequelae that are limited to a single lobe (choice B is incorrect.)
Pulmonary thromboembolism should produce no change or produce areas of relative lucency on the chest radiograph rather than the localized area of higher attenuation in the right lower lobe that was seen in this patient (choice C is incorrect.)

Reperfusion pulmonary edema is a complication of pulmonary thromboendarterectomy that occurs in approximately 30% of patients, typically in regions where proximal chronic thromboemboli have been resected (choice D is correct). The diagnosis is suggested by the chest radiograph showing airspace disease in the right lower lobe, where the patient's most significant lesions were removed (Figure 4). Although not generally ordered in the acute setting, a repeat radionuclide perfusion scan was obtained in this patient and showed increased blood flow and exudation of the tracer into alveolar spaces of the right lower lobe, further confirming the diagnosis (Figure 5).
Reperfusion pulmonary edema typically develops within the first 72 h after pulmonary thromboendarterectomy or balloon pulmonary angioplasty and can range in severity from mild to life-threatening. Treatment is largely supportive, with supplemental oxygen; mechanical ventilation; and, in severe cases, extracorporeal membrane oxygenation. Some data suggest that inhaled vasodilators may be beneficial, presumably by dilating vasculature in better ventilated portions of the lung to improve ventilation-perfusion matching and by shunting blood flow away from injured areas of the lung, thus decreasing pulmonary edema formation due to reperfusion in those areas. Unfortunately, there is no mechanism to identify preoperatively the precise risk of reperfusion pulmonary edema in a specific patient, and the complication is not reduced by prophylactic low tidal volume ventilation vs higher tidal volumes.

A 51-year-old man develops progressive dyspnea on exertion and an extensive evaluation diagnoses chronic thromboembolic pulmonary hypertension, with a radionuclide perfusion scan showing particularly reduced blood flow to the right lower lobe (Figure 1). His medical history is notable only for essential hypertension, for which he is treated with losartan. He undergoes a technically challenging pulmonary
thromboendarterectomy, with removal of endovascular material (Figure 2). Approximately 6 h after the operation, the patient is still mechanically ventilated and is noted to have an increasing oxygen requirement. A repeat chest radiograph is obtained (Figure 3).

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بسم الله الرحمن الرحيم
Today lecture

Many thanks for Dr Emad Efat

Many thanks for Dr Mohamad Zakaria

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Driving pressure (DP) is the pressure required to tidally distend and inflate the alveolar structures. It is a static measurement
(plateau pressure minus PEEP) that reflects only compliance properties of the respiratory system during tidal breath delivery,
not flow resistive properties. Mathematically, DP is tidal volume/compliance (Vt/C).
Excessive tidal stretch (strain) of alveolar structures during mechanical ventilation can produce ventilator-induced lung injury
(VILI). A practical way to address this is the use of “normal” tidal volumes based on ideal lung size (ie, 5-7 mL/kg IBW).
However, this may be too simplistic in lungs with extensive regional consolidation. Under these conditions, the volume of lung
capable of being ventilated may be markedly reduced (“baby lungs”). Thus, delivery of a normal-sized Vt based on IBW may
produce excessive regional tidal stretch in the reduced functional lung. Because compliance may be considered a surrogate for
functional lung size, DP has been proposed as a tool to more appropriately scale Vt.
A threshold for a “safe” DP is not clear. Retrospective analyses of multiple randomized clinical trials (most of which were
evaluating PEEP strategies, not Vt settings) have suggested that DP values <15 cm H2O seem safer than higher values.
Recommendations to keep DP below this threshold have been made by several authorities. In our patient, the DP is 29
(plateau pressure) – 12 (PEEP) or 17 cm H2O. Given the choices offered, the only way to reduce the DP would be to reduce the
Vt (choice A is correct; choice D is incorrect).

Another way to perhaps reduce DP in our patient might be to improve compliance with PEEP. A novel way to assess this
is to measure a stress index. This parameter is the slope of the airway pressure graphic during inflation with a volume
controlled breath (no patient effort) using a constant inspiratory flow. Under these conditions, the airway pressure slope
represents respiratory system compliance during the tidal breath. If it slopes upward (worsening compliance) it suggests
tidal overdistention. If it slopes downward (improving compliance) it suggests recruitment during the tidal volume. Ideally,
the slope should be linear, suggesting a stable compliance during the tidal breath. Three examples are given in Figure 39-A.
However, in the case presented, the only PEEP choice given was to inappropriately eliminate it (choice B is incorrect).
Respiratory rate adjustments in the presence of adequate expiratory times will have no effect on DP (choice C is incorrect).
Importantly, using DP to target tidal volumes settings has not been subjected to a prospective randomized trial as yet. Such a
trial would randomize patients with a plateau pressure <30 cm H2O and receiving a Vt of 6 mL/kg IBW but with a high DP to
either remain on 6 mL/kg or have the Vt reduced further to reduce DP.

اجابة السؤال 👇🏼👇🏼👇🏼
A

A 45-year-old woman is requiring mechanical ventilation for a bilateral aspiration pneumonia following several days of
heavy alcohol intake. She is receiving volume-controlled ventilation with a tidal volume of 6 mL/kg ideal body weight (IBW),
a rate of 18 (adequate expiratory time present), a PEEP of 12 cm H2O and an Fio2 of 0.40. Her pH is 7.39, Pco2 is 43 mm Hg,
and Po2 is 69 mm Hg. The peak pressure on the ventilator is 35 cm H2O and the plateau pressure is 29 cm H2O. Although
these settings reflect current “lung protective” management, you would also like to optimize a newly described parameter—the
driving pressure—in accordance with some recent observational data and expert recommendations.

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Many thanks for Dr Ahmad Bashir

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Today lecture

The Centers for Disease Control recommend prompt initiation of empiric treatment of influenza (ie, within 48 hours of
illness onset) in women who are pregnant or postpartum and have flu symptoms because they are at particularly increased
risk of serious complications. The neuraminidase inhibitors oseltamavir and zanamivir are considered safe and effective in
pregnancy; oseltamavir is preferred because more data are available to assess the risks and benefits (choice C is correct; choice
D is incorrect).
While influenza vaccines are recommended for all pregnant women, they reduce the risk of infection by only around 50%.
Therefore, the assumption that this patient’s symptoms are not caused by influenza because she was vaccinated is incorrect,
and treatment should be started promptly regardless of vaccination status (choice A is incorrect). While a rapid influenza
diagnostic test (RIDT) yields a result in around 15 min and is highly specific for the diagnosis, these tests are only 50% to 70%
sensitive and more likely to yield false negatives when flu is more prevalent in the community. Therefore, this patient should
be treated regardless of the result of the RIDT (choice B is incorrect).

اجابة السؤال 👇🏼👇🏼👇🏼
C

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Today lecture

A 32-year-old woman at 30 weeks gestation calls because she has 1 day of cough, temperature of 38°C, sore throat, and
myalgia. She has no sick contacts, but there are cases of influenza in the community. She had an influenza vaccine 1 month
before.

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The treatment and prevention of herpes zoster focus on reducing symptom severity, preventing complications, and managing post-herpetic neuralgia (PHN):

Prevention:
Zoster vaccine: Recommended for people aged 60 and above to lower the risk of herpes zoster and PHN. Contraindicated in immunosuppressed patients.

General Measures:
Rest and adequate pain management.

Apply protective ointments like petroleum jelly to the rash.

Use oral antibiotics for secondary bacterial infections if needed.

Specific Measures:
Antiviral therapy: Early initiation (within 1–3 days of symptom onset) with aciclovir, valaciclovir, or famciclovir to reduce pain and symptom duration.

Systemic steroids are of unproven benefit.

Management of post herpetic neuralgia :
Early antiviral use to prevent its onset.

Options include local anesthetic applications, topical capsaicin, tricyclic antidepressants (e.g., amitriptyline), anti-epileptic drugs (gabapentin or pregabalin), and procedures like transcutaneous electrical nerve stimulation, acupuncture, or botulinum toxin injections.

NSAIDs and opioids are generally ineffective for PHN relief.

Timely diagnosis and early treatment are essential to minimize complications and improve patient outcomes.

What are the clinical features of herpes zoster?

Herpes zoster is characterized by a dermatomal distribution of painful, blistering rashes typically confined to one or two adjacent sensory nerves, with a sharp boundary at the anterior and posterior midlines. The condition often begins with localized pain, fever, and lymph node tenderness, followed by the appearance of red papules that evolve into blisters. Commonly affected regions include the thoracic, cervical, ophthalmic, and lumbar/sacral dermatomes. Recovery typically occurs within 2–4 weeks, depending on the patient's age and overall health, with some cases presenting atypically, such as pain without rash or rash without pain.

Complications...
Dermatomal extension: Involvement of multiple or bilateral dermatomes.

Ophthalmic involvement: Eye complications when the ophthalmic branch of the trigeminal nerve is affected.

Prolonged healing: Deep blisters with potential scarring.

Neurological issues: Muscle weakness, most notably facial nerve palsy (e.g., Ramsay Hunt syndrome), with variable recovery outcomes.

Systemic involvement: Rare infections of internal organs like the brain, lungs, or gastrointestinal tract.

Infectious risk: Contagion to individuals who have not had chickenpox.

Herpes zoster in pregnancy may harm the fetus or newborn, though such cases are uncommon.

Post-herpetic neuralgia (PHN): A persistent, often severe pain, or itching following the rash, especially in older adults or facial infections.

Who gets herpes zoster?
Anyone who has had varicella (chickenpox) may subsequently develop herpes zoster. Zoster can occur in childhood but is much more common in adults, especially older people. People with various kinds of cancer have a 40% increased risk of developing zoster. People who have had zoster rarely get it again; the chance of getting a second episode is about 1%.

Herpes zoster often affects people with weak immunity.

What causes herpes zoster?
After primary infection—varicella—VZV remains dormant in dorsal root ganglia nerve cells in the spine for years before it is reactivated and migrates down sensory nerves to the skin to cause herpes zoster.

It is not clear why herpes zoster affects a particular nerve fibre. Triggering factors are sometimes recognised, such as:

Pressure on the nerve roots
Radiotherapy at the level of the affected nerve root
Spinal surgery
An infection
An injury (not necessarily to the spine)
Contact with someone with varicella or herpes zoster

Herpes zoster🔥💥

What is herpes zoster?
Herpes zoster is a localised, blistering and painful rash caused by reactivation of varicella-zoster virus (VZV). Herpes zoster is also called shingles.

VZV is also called herpesvirus 3 and is a member of the Herpesvirales order of double-stranded DNA viruses.

The chest radiograph shows a mass in the right lower lobe (Figure 3). In a smoker, this suggests the diagnosis of lung cancer. Pain and swelling over the long bones would most likely be due to hypertrophic osteoarthropathy (HOA). The 99mTc bone scan is the most sensitive diagnostic test, the isotope concentrating in areas of the increased osteoblastic activity and subperiosteal new bone formation that characterizes the condition (Figure 2) (choice C is correct). The diagnosis may also be established when radiography shows new bone proliferation in the long bones, especially the radius, ulna, tibia, and fibula (Figure 4). Although the 18FDG-PET scan will show hypermetabolic activity in the same areas, this test is neither as sensitive nor specific in the diagnosis of HOA as the radionuclide scan (choice D is incorrect).
A rare primary inherited form of HOA usually has autosomal dominant transmission. The secondary form is usually associated with lung and pleural conditions, most often non-small cell lung cancer; patients with malignant mesothelioma and benign fibrous tumors of the pleura may have HOA. HOA is also associated with other lung diseases, including pulmonary fibrosis and bronchiectasis, cyanotic congenital heart disease, gastrointestinal tumors, cirrhosis, and inflammatory bowel disease. Patients who have clubbing associated with nonmalignant disorders rarely have HOA. HOA does not preclude curative surgery of lung cancer; these patients should have the same staging evaluation and treatment as patients who do not have HOA, and resection of the tumor often leads to remission of osteoarthropathy. HOA without clubbing may occasionally be the presenting symptom in patients with lung cancer, as in this case.
The pathogenesis of HOA is not known but probably involves humoral factors that promote growth of vascular connective tissue and new bone formation. Neural factors are also probably involved, as some cases of vagotomy on the side of an inoperable lung cancer have led to remission of osteoarthropathy.
HOA sometimes resembles rheumatoid arthritis clinically, but not in this case where respiratory symptoms and not joint pains and swelling are most prominent. Serum anti-CCP antibodies are highly specific for the diagnosis and useful to predict the development of more severe disease but are not increased in HOA (choice A is incorrect). Serum parathyroid hormone-related protein accounts for hypercalcemia, the most common paraneoplastic syndrome occurring in patients with squamous cell carcinoma of the lung, but this patient has no symptoms of hypercalcemia (choice B is incorrect).

اجابة السؤال 👇🏼👇🏼👇🏼
C

A 52-year-old woman presents with pain and swelling of both knees, ankles, and pretibial areas. She has smoked 1.5 packs of cigarettes daily for the past 35 years and has a chronic productive cough that has not changed in the last several years. Physical exam is remarkable for bilateral rhonchi and wheezes, and there is an absence of digital clubbing. The chest radiograph is shown in (Figure 1), and radiographs of the lower extremities are normal.

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Today lecture

https://t.me/pulmolectures

This patient has stable severe COPD though remains symptomatic despite optimal medical therapy and pulmonary
rehabilitation. Interventional therapy to treat COPD should be considered and, in this patient, bronchoscopic placement of an
endobronchial valve is the most appropriate option (choice B is correct). One-way endobronchial valves (EBVs) are placed in
hyperinflated lung regions, allowing trapped air to exit and preventing inhaled air from flowing back in. To be effective, EBVs
need to be placed in areas of little to no collateral ventilation to increase the likelihood that these areas will remain collapsed
and essentially achieve lung volume reduction. Techniques to measure collateral airflow include a physiologic assessment
using endoscopic balloon occlusion, or the finding of fissure integrity on HRCT. Visualization of >90% of a fissure between the
lobe targeted for treatment and the adjacent lobe on at least one axis implies the absence of significant collateral ventilation,
as was the case in this patient, making EBV a reasonable option. Interoperator variability, however, is noted with the fissure
integrity method, and should not be used alone to assess collateral ventilation. When used along with the balloon occlusion
method, there is greater predictability of lobar collapse after EBV placement.
Initial studies of EBVs showed modest benefits in lung function, though when patients without interlobar collateral ventilation
were selected out, bronchoscopic EBV treatment significantly improved lung function, exercise capacity, and quality of life
in patients with severe emphysema, compared with usual care. This is likely due to a decrease in thoracic volume leading to
improved mechanical efficiency of the lung and respiratory muscles. EBVs have been shown to be effective in patients with
both heterogeneous and homogenous emphysema.
One complication of EBV placement is pneumothorax, which typically occurs in the first 2 days after the procedure and may
be a result of ruptured blebs or bullae due to rapid shifts in lung volumes. Other complications include the need for repeat
bronchoscopy to either remove a valve (eg, due to recurrent pneumothorax, torsion) or replace a valve (eg, due to migration,
valve dislocation).
Further studies are needed to define optimal patient selection. Patients who undergo EBV placement remain candidates for
future LVRS or lung transplant.
Lung volume reduction surgery where dead space is essentially surgically removed, is reasonable to consider given her
persistent symptoms despite optimal treatment, evidence of air trapping on lung function studies, and heterogeneously
distributed emphysema. Evidence of pulmonary hypertension (mean pulmonary artery pressure ≥35 mm Hg), however, is a
contraindication (choice A is incorrect).
This patient would not be a candidate for a lung or heart-lung transplant based on the diagnosis of malignancy within the past
2 years (choices C and D are incorrect). In addition, consideration for lung transplant in patients with COPD should occur
when the FEV1 is <25% of predicted, and heart-lung transplant should be considered when there is also a history of refractory
end-stage heart disease, both of which are not the case in this patient.

اجابة السؤال 👇🏼👇🏼👇🏼
B

A 63-year-old woman with a history of emphysema reports persistent dyspnea despite treatment with a combination
inhaled steroid/long-acting beta-agonist and a long-acting muscarinic antagonist, and an intensive pulmonary rehabilitation
program. She has had no recent exacerbations. Past medical history includes breast cancer diagnosed 1 year ago; she tolerated
a lumpectomy without respiratory complications. Cardiopulmonary assessment is shown in Table 35-A.
High-resolution CT scan (HRCT) scan of the chest shows upper lung zone predominant emphysema and a complete
interlobar fissure on coronal and sagittal views.

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This patient has pneumonitis due to treatment with pembrolizumab, an immune checkpoint inhibitor (ICI). ICI pneumonitis is a diagnosis of exclusion and requires the rejection of other diagnostic possibilities including infection, pulmonary edema, pulmonary embolism, and exacerbation of chronic respiratory disease. ICI pneumonitis is graded from 1-5 (see Figure 9). Withholding of ICI therapy and, for grade 2 or higher toxicity, administration of glucocorticoids are the cornerstones of therapy for ICI pneumonitis. While most patients with ICI pneumonitis respond to these interventions, a minority, such as this patient, experience progression to life-threatening respiratory failure. While data are limited, addition of an additional immunosuppressive agent such as infliximab (with or without cyclophosphamide) or mycophenolate is generally indicated (choice B is correct). This patient improved clinically after infliximab was added, and follow-up chest CT images obtained approximately 12 weeks after treatment are shown in Figures 10-12. The incidence of ICI pneumonitis is approximately 5% and is lower in patients treated with an ICI combination that includes an anti-programmed cell death protein 1 or anti-programmed cell death ligand 1 monoclonal antibody (3%) than in patients treated with an ICI combination that includes an anti-cytotoxic T-lymphocyte antigen 4 antibody (10%). The incidence of the most severe forms of ICI pneumonitis (grade ≥3) is slightly below 1%. The timing of ICI pneumonitis is variable, with a median onset of symptoms of 2.8 months after treatment. The choice to reinitiate ICI therapy after toxicity has occurred is complex and dependent on multiple factors, including the severity of the toxicity, the degree of responsiveness to immunosuppressive agents, and the availability of non-ICI treatment options.

External beam radiotherapy does not have a role in the treatment of ICI pneumonitis (choice C is incorrect). ICI treatment has been associated with exacerbation of radiation pneumonitis and has induced recall radiation pneumonitis in previously irradiated lung fields up to 2 years after radiotherapy has been administered.

Therapeutic plasma exchange is a technique in which a patient's blood is removed and then returned with their own formed blood elements but with donor plasma substituted for their own plasma, which has been removed and discarded. It is useful in the treatment of a variety of autoantibody-related conditions such as acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré syndrome), anti-glomerular basement membrane disease (Goodpasture syndrome), myasthenic crisis, and some types of vasculitis; however, it does not have a role in the treatment of ICI pneumonitis (choice D is incorrect).

Cyclosporine is a calcineurin inhibitor that reduces the production of IL-2 and several other cytokines in T-lymphocytes. While calcineurin inhibitors such as cyclosporine and tacrolimus are cornerstones of immunosuppression among solid organ transplant recipients, they do not have a role in the management of ICI pneumonitis (choice A is incorrect).

إجابة السؤال 👇🏼👇🏼👇🏼
B

Many thanks for Dr Mohamed AlsayedSadek

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بسم الله
سؤال اليوم 👇🏼👇🏼👇🏼

A 71-year-old man with gastric adenocarcinoma presents with progressive cough and dyspnea approximately 3 months after beginning pembrolizumab therapy. He reports no fevers and does not feel subjectively ill. Physical examination is notable for SpO2 of 90% on ambient air. Breath sounds are normal, and rare scattered, nondependent crackles are heard. There is no dependent edema. His anteroposterior chest radiograph and representative chest CT images are shown in Figures 1-4.

An echocardiogram shows normal cardiac function, and the findings of extensive evaluation for infection, including bronchoscopy with bronchoalveolar lavage, are negative. Despite negative fluid balance, empiric antimicrobial treatment (vancomycin, piperacillin-tazobactam, azithromycin, and micafungin), and treatment with high-dose methylprednisolone, the patient's oxygen requirement and dyspnea continue to progress. A repeat anteroposterior chest radiograph and representative chest CT imaging from 7 days later are shown in Figures 5-8, and shortly after the CT imaging is obtained, he requires intubation and mechanical ventilation.