Anwser,s 12

Wednesday, April 12, 2023

Anwser,sDr :ANAS SAHLE

1. Chest xr cases.2. Chest clinical case.

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chest xr casesDr :anas sahle

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CXR61

Child present with cough\tachypnea\fever

Croup.


Croup.• also called acute laryngotracheobronchitis is

due to viral infection of the upper airway by parainfluenza virus or respiratory syncytial virus (RSV)

http://radiopaedia.org/articles/missing?article%5Btitle%5D=respiratory-syncytial-virus-rsv



CXR62a

Sign name is: The spinnaker sign (also known as the angel wing sign)

is a sign of pneumomediastinum seen on neonatal chest radiographs. It refers to the thymus being outlined by air with each lobe displaced laterally and appearing like spinnaker sails.

http://radiopaedia.org/articles/pneumomediastinum

http://radiopaedia.org/articles/thymus

CXR62b

CXR63

Sign name is: bulging fissure sign


bulging fissure sign • The bulging fissure sign refers to lobar

consolidation where the affected portion of the lung is expanded.

• It is now rarely seen due to the widespread use of antibiotics.

• The most common infective causative agents are

– Klebsiella pneumoniae– Streptococcus pneumoniae– Pseudomonas aeruginosa– Staphylococcus aureus

http://radiopaedia.org/articles/air-space-opacification-1

CXR64

Name is: paraspinal lines

CXR65

Name is: Azygous vein

CXR66

Name is :AP window

CXR67Name is: paratracheal "stripe "

CXR68a

CXR68b

Diagnosis is:Allergic bronchopulmonary aspergillosis (ABPA)

CXR69

Name is : pleuralplaques

http://radiopaedia.org/articles/pleural-plaque

http://radiopaedia.org/articles/pleural-plaque

CXR70

Cardiac patient take anti-arrythmatic drug:Amiodarone lung


chest clinical casesA 60-Year-Old Man with

Acute Respiratory Failure and Mental Status ChangesSubmitted by

Lokesh Venkateshaiah, MDFellowDivision of Pulmonary, Critical Care and Sleep MedicineThe MetroHealth System, Case Western Reserve UniversityCleveland, OhioBruce Arthur, MDFellowDivision of Pulmonary, Critical Care and Sleep MedicineThe MetroHealth System, Case Western Reserve UniversityCleveland, OhioJ. Daryl Thornton, MD, MPHAssistant ProfessorDivision of Pulmonary, Critical Care and Sleep Medicine, Center for Reducing Health DisparitiesThe MetroHealth System, Case Western Reserve UniversityCleveland, Ohio


History • A 60-year-old man presented to the emergency department complaining of persistent right-

sided chest pain and cough. • The chest pain was pleuritic in nature and had been present for the last month. • The associated cough was productive of yellow sputum without hemoptysis. • He had unintentionally lost approximately 30 pounds over the last 6 months and had

nightly sweats. • He had denied fevers, chills, myalgias or vomiting. • He also denied sick contacts or a recent travel history. • He recalled childhood exposures to persons afflicted with tuberculosis. • The patient smoked one pack of cigarettes daily for the past 50 years and denied

recreational drug use. • He reported ingesting twelve beers daily and had had delirium tremens, remote right-sided

rib fractures and a wrist fracture as a result of alcohol consumption. • He had worked in the steel mills but had discontinued a few years previously. • He collected coins and cleaned them with mercury. • The patient’s past medical history was remarkable for chronic “shakes” of the upper

extremities for which he had not sought medical attention. • Other than daily multivitamin tablets, he took no regular medications.


Hospital course• He was initially admitted to the general medical floor for treatment of

community-acquired pneumonia (see Figure 1) and for the prevention of delirium tremens.

• He was initiated on ceftriaxone, azithromycin, thiamine and folic acid. • Diazepam was initiated and titrated using the Clinical Institute

Withdrawal Assessment for Alcohol Scale (CIWAS-Ar), a measure of withdrawal severity .

• By hospital day 5, his respiratory status continued to worsen, requiring transfer to the intensive care unit (ICU) for hypoxemic respiratory failure.

• His neurologic status had also significantly deteriorated with worsening confusion, memory loss, drowsiness, visual hallucinations (patient started seeing worms) and worsening upper extremity tremors without generalized tremulousness despite receiving increased doses of benzodiazepines.


Physical Exam• On arrival at the medical ICU, the patient appeared cachectic and dyspneic. • He was unable to complete sentences. • His blood pressure was 125/71 mm Hg, heart rate of 122/min, temperature 100 °F,

respiratory rate 33/min, and oxygen saturation 77% on room air and 92% on 40% venti-mask.

• At the time of presentation to the hospital he had oxygen saturation of 92% on room air.

• The heart exam revealed tachycardia but regular rhythm, a normal S1 and S2 and no murmurs, gallops or rubs.

• On auscultation of the lung fields, breath sounds were diminished on the right side in the upper zone without the presence of adventitious sounds. The abdomen was benign without organomegaly.

• The patient’s extremities were normal with absence of clubbing or edema. • He was oriented only to person, and had an inability to pay attention or remember

immediate events. • He was moving all four extremities with slightly brisk deep tendon reflexes. • Neck was supple and the pupils were brisk in reacting to light.


Lab• White blood cell count was 11,000/mm3 with 38% neutrophils, 8% lymphocytes, 18 % monocytes and 35%

bands• Hematocrit 33%• Platelet count was 187,000/mm3

• Serum sodium was 125 mmol/L, potassium 3 mmol/L, chloride 91 mmol/L, bicarbonate 21 mmol/L, • blood urea nitrogen 14 mg /dl, serum creatinine 0.6 mg/dl and anion gap of 14.• Urine sodium <10 mmol/L, urine osmolality 630 mosm/kg• Liver function tests revealed albumin 2.1 with total protein 4.6, normal total bilirubin, aspartate transaminase

(AST) 49, Alanine transaminase (ALT) 19 and alkaline phosphatase 47.• Three sputum samples were negative for acid-fast bacilli (AFB).• Bronchoalveolar lavage (BAL) white blood cell count 28 cells/µl, red blood cell count 51 cells/µl, negative for

AFB and negative Legionella culture. • BAL gram stain was without organisms or polymorphonuclear leukocytes.• Blood cultures were negative for growth.• Sputum cultures showed moderate growth of Pasteurella multocida.• 2D transthoracic ECHO of the heart showed normal valves and an ejection fraction of 65% with a normal left

ventricular end-diastolic pressure and normal left atrial size. No vegetations were noted.• Purified protein derivative (PPD) administered via Mantoux testing was 8 mm in size at 72 hr after placement.• Human immunodeficiency virus (HIV) serology was negative. • Arterial blood gas (ABG) analysis performed on room air on presentation to the ICU: pH 7.49, PaCO2 29 mm

Hg, PaO2 49 mm Hg.


cxr

(Figure 1.1) Figure 1.2 .


Question 1• As this patient’s acute respiratory failure

worsens, what is the appropriate means to provide ventilatory support?

• A. Pressure support ventilation • B. Volume assist-control ventilation with tidal

volumes of 6 ml/kg predicted body weight • C. Volume assist-control ventilation with tidal

volumes of 12 ml/kg predicted body weight • D. Noninvasive positive pressure ventilation


discussion• After admission to the ICU, the patient was noted to be in acute lung injury (ALI), a subset of acute

respiratory distress syndrome (ARDS). • The diagnosis of ALI requires all three of the following: (a) bilateral pulmonary infiltrates, (b) a

PaO2:FiO2 ratio of ≤ 300 and (c) echocardiographic evidence of normal left atrial pressure or pulmonary-artery wedge pressure of ≤ 18 mm Hg.

• Low tidal volume ventilation (LTVV), also known as lung protective ventilation, has been demonstrated to significantly improve mortality in patients with ALI and ARDS .

• In a study conducted by the ARDS Network comparing LTVV to traditional tidal volumes, patients were placed either on tidal volumes of 12 ml/kg predicted body weight or 6 ml/kg predicted body weight within 4 hr following randomization.

• Tidal volumes in the 12 ml/kg group were reduced to as low as 4 ml/kg while keeping the plateau pressure ≤ 50 cm H2O, and tidal volumes in the 6 ml/kg group were reduced to as low as 4ml/kg while keeping the plateau pressure ≤ 30 cm H2O.

• The trial was discontinued early because of the mortality difference between the two groups (31% in the 6 ml/kg group versus 40% in the 12 ml/kg group, p = 0.007).

• Ventilator-free days were also significantly higher in the LTVV group.• While patients with ALI and ARDS can be maintained with pressure-limited or volume-limited modes

of ventilation, only volume assist-control ventilation was utilized in the ARDS Network multicenter randomized controlled trial that demonstrated a mortality benefit.

• Noninvasive ventilation has not been demonstrated to be superior to endotracheal intubation in the treatment of ARDS or ALI and is not currently recommended .


Question 2• What is the most likely explanation for

his altered mental status?• A. Alcoholic hallucinosis • B. Pneumonia and sepsis • C. Heavy metal poisoning • D. Frontal lobe stroke


discussion• This is a case of heavy metal poisoning with mercury. • The patient used mercury to clean coins. • Family members who had visited his house while he was hospitalized found several jars of mercury throughout

his home. • The Environmental Protection Agency (EPA) was notified and visited the home. • They found aerosolized mercury levels of > 50,000 PPM and had the home immediately demolished. • Alcoholic hallucinosis is a rare disorder occurring in 0.4 - 0.7% of alcohol-dependent inpatients (5). • Affected persons experience predominantly auditory but occasionally visual hallucinations. • Delusions of persecution may also occur. • However, in contrast to alcohol delirium, other alcohol withdrawal symptoms are not present and the

sensorium is generally unaffected.• Delerium tremens (DT) occurs in approximately 5% of patients who withdraw from alcohol and is associated

with a 5% mortality rate. • DT typically occurs between 48 and 96 hr following the last drink and lasts 1-5 days. • DT is manifested by generalized alteration of the sensorium with vital sign abnormalities. • Death often results from arrhythmias, pneumonia, pancreatitis or failure to identify another underlying

problem .• While DT certainly could have coexisted in this patient, an important initial step in the management of DT is to

identify and treat alternative diagnoses.• Delirium is frequent among older patients in the ICU (7), and may be complicated by pneumonia and sepsis. • However, pneumonia and sepsis as causes for delirium are diagnoses of exclusion and should only be attributed

after other possibilities have been ruled out.


Contin-• Frontal lobe stroke is unlikely, given the absence of other findings in the history or physical

examination present to suggest an acute cerebrovascular event. • In 1818, Dr. John Pearson coined the term erethism for the characteristic personality changes

attributed to mercury poisoning .• Erethism is classically the first symptom in chronic mercury poisoning .• It is a peculiar form of timidity most evident in the presence of strangers and closely

resembles an induced paranoid state. • In the past, when mercury was used in making top hats, the term “mad as a hatter” was used

to describe the psychiatric manifestations of mercury intoxication. • Other neurologic manifestations include tremors, especially in patients with a history of

alcoholism, memory loss, drowsiness and lethargy. • All of these were present in this patient. • Acute respiratory failure (ALI/ARDS) can occur following exposure to inhalation of mercury

fumes • Mercury poisoning has also been associated with acute kidney injury .• Although all of the options mentioned above could possibly contribute to the development

of delirium, only mercury poisoning would explain the constellation of findings of confusion, upper extremity tremors, visual hallucinations, somnolence and acute respiratory failure (ALI/ARDS).


Question 3• The most likely form of mercury intoxication

that could explain this patient’s clinical picture would be:

• A. Inorganic mercury • B. Elemental mercury• C.Organic mercury • D. Methylmercury


discussion• Knowledge of the form of mercury absorbed is helpful in the management of such patients, as each has

its own distinct characteristics and toxicity. • There are three types of mercury: elemental, organic and inorganic. • This patient had exposure to elemental mercury from broken thermometers. • Elemental mercury is one of only two known metals that are liquid at room temperature and has been

referred to as quicksilver (.• It is commonly found in thermometers, sphygmomanometers, barometers, electronics, latex paint, light

bulbs and batteries . • Although exposure can occur transcutaneously or by ingestion, inhalation is the major route of toxicity. • Ingested elemental mercury is poorly absorbed and typically leaves the body unchanged without

consequence (bioavailability 0.01% [13]). • However, inhaled fumes are rapidly absorbed through the pulmonary circulation allowing distribution

throughout the major organ systems. • Clinical manifestations vary based on the chronicity of the exposure . • Mercury readily crosses the blood-brain barrier and concentrates in the neuronal lysosomal dense bodies. • This interferes with major cell processes such as protein and nucleic acid synthesis, calcium homeostasis

and protein phosphorylation. • Acute exposure symptoms manifest within hours as gastrointestinal upset, chills, weakness, cough and

dyspnea.


Contin-• Inorganic mercury salts are earthly-appearing, red ore found historically in cosmetics and

skin treatments. • Currently, most exposures in the United States occur from exposure through germicides or

pesticides . • In contrast to elemental mercury, inorganic mercury is readily absorbed through multiple

routes including the gastrointestinal tract. • It is severely corrosive to gastrointestinal mucosa (. • Signs and symptoms include profuse vomiting and often-bloody diarrhea, followed by

hypovolemic shock, oliguric renal failure and possibly death .• Organic mercury, of which methylmercury is an example, has garnered significant attention

recently following several large outbreaks as a result of environmental contamination in Japan in 1956 (17) and grain contamination in Iraq in 1972 .

• Organic mercury is well absorbed in the GI tract and collects in the brain, reaching three to six times the blood concentration .

• Symptoms may manifest up to a month after exposure as bilateral visual field constriction, paresthesias of the extremities and mouth, ataxia, tremor and auditory impairments .

• Organic mercury is also present in a teratogenic agent leading to development of a syndrome similar to cerebral palsy termed "congenital Minamata disease" .


Question 4• The best way to diagnose mercury toxicity in

this patient is to:• A. Sample hair for levels of mercury • B. Measure blood levels of mercury • C. Measure 24-hr urine levels of mercury• D. Measure spot urine levels of mercury


discussion• The appropriate test depends upon the type of mercury to which a patient has been

exposed. • After exposure to elemental or inorganic mercury, the gold standard test is a 24-hr urine

specimen for mercury. • Spot urine samples are unreliable. • Urine concentrations of greater than 50 μg in a 24-hr period are abnormal (21). • This patient’s 24-hr urine level was noted to be 90 μg. • Elemental and inorganic mercury have a very short half-life in the blood.• Exposure to organic mercury requires testing hair or whole blood. • In the blood, 90% of methyl mercury is bound to hemoglobin within the RBCs. • Normal values of whole blood organic mercury are typically < 6 μg/L. This patient’s whole

blood level was noted to be 26 μg/L. • This likely reflects the large concentration of elemental mercury the patient inhaled and

the substantial amount that subsequently entered the blood.• Mercury levels can be reduced with chelating agents such as succimer, dimercaprol (also

known as British anti-Lewisite (BAL)) and D-penicillamine, but their effect on long-term outcomes is unclear (22-25).


chest ct cases-11Dr :anas sahle

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HRCT-1

HRCT-1

• Give the distribution and pattern of the nodules in the right lower lobe?

• Centrilobular nodules with tree-in-bud pattern

• Find the collapsed right middle lobe. • Find the collapsed lingula.

HRCT-1

• Find a row of 3 centrilobular nodules in the right lung.

• Find 2 examples of tree-in-bud pattern in the right lung.

• Find a thickened bronchus, consistent with bronchitis in the right lung.

HRCT-1

Gross Appearance

• This lung from a young child with cystic fibrosis shows the volume loss and atelectasis (red areas) associated with bronchiectasis.

• The paler, aerated lung bulges above the areas of collapse. • This lung did not collapse when it was removed postmortem

as a normal lung would.

• Why would the aerated portions of lung remain expanded?

• The widespread bronchitis and bronchiolitis produce variable obstruction of small airways with mucus and exudate, which trap air.

• Here, the posterior mid lung shows extensive varicose bronchiectasis, which is similar to that seen in the HRCT image in the right middle lobe.

• The term varicose denotes dilation as seen in venous varices.

• When greater dilation occurs, it is referred to descriptively as cystic bronchiectasis

• Note the loss of parenchyma between the crowded airways, and the large caliber of the lumen near the pleural surface, compared to airways in the lower lung.

• Find a bronchiectatic airway.• Find a normal airway in the lower lung.

Histologic Changes

• This is a subsegmental bronchus from a patient with bronchiectasis.

• Describe the structures in the wall.• Fibrous tissue and inflammation. The cartilage and smooth muscle have been

destroyed.

• Describe the contents of the lumen.• Purulent exudate

• How does alveolar parenchymal loss occur?• Chronic peribronchial inflammation gradually replaces alveoli with scar.

• How does airway obstruction occur? – 1) Mucus and exudate in large airways and – 2) stenosing mural fibrosis and luminal inflammation of small airways.

Differential diagnosis

• Differential diagnosis of bronchiectasis, bronchitis, and bronchiolitis on HRCT:– chronic bacterial or mycobacterial infections, – cystic fibrosis, – allergic bronchopulmonary aspergillosis, –middle lobe syndrome, – chronic bronchiolitis.– proximal bronchial obstruction by tumor or

foreign body.

Histologic differential diagnosis:

• chronic bacterial or mycobacterial infections.• cystic fibrosis.• allergic bronchopulmonary aspergillosis. • middle lobe syndrome. • chronic bronchiolitis.• proximal bronchial obstruction by tumor or

foreign body.

Diagnosis:

Bronchiectasis with associated adjacent bronchitis and bronchiolitis.

Diagnostic features

• Diagnostic features of bronchiectasis, bronchitis, and bronchiolitis on HRCT:–Bronchial dilation and wall thickening – Tree-in-bud pattern –Centrilobular nodules –Mosaic perfusion of air trapping (more

later).


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