Pathologie der Atemwege

Clinical HistoryThis 47 year old woman was admitted with terminal carcinomatosis. On examination a hard liver and a right pelvic mass were palpable. She had been ill with constitutional symptoms for months and she finally sought medical attention. She was admitted for palliative care and died shortly afterwards.Pathology The left lung has been sliced longitudinally to display the cut surface. Multiple pale tumour nodules of varying size are scattered throughout the lung substance. Near the hilum several nodules are confluent. The hilar lymph nodes contain pale tumour tissue. Small tumour nodules can be seen beneath the thickened pleura. Histologically these were metastatic deposits of adenocarcinoma. At post-mortem there was an adeno-carcinoma of ovary, with metastases in lungs, heart, liver and pericardium.Further InformationPulmonary metastases are more common than primary lung cancer. Malignant disease arising anywhere in the body may spread to the lungs. Sarcomas usually metastasize by the bloodstream, and carcinomas spread either via the bloodstream or the lymphatic system or both.

Clinical HistoryA 47-year-old male presents with a 13-month history of dysphonia and odynophagia at the level of his thyroid cartilage. He has a significant smoking history. Investigations revealed a laryngeal tumour. He received radiotherapy to the tumour followed by a laryngectomy. Six months later pulmonary metastases were discovered, and he subsequently died.Pathology This is the patient’s laryngectomy specimen. The larynx has been sliced open and is viewed from the posterior aspect. There is significant right vocal cord distortion by an irregular ulcerating tumour. Mucosal congestion is also noted. Histologically this was a well differentiated squamous cell carcinoma (SCC).Further InformationOver 95% of laryngeal cancers are SCC. The tumour usually develops on the vocal cords but may occur above or below the cords, on the epiglottis, aryepiglottic folds or in the pyriform sinuses. The cancer usually begins as carcinoma in situ, progressing to ulcerated and fungating carcinoma with continued exposure to carcinogens.The greatest risk factors for developing cancer of the larynx are tobacco smoke and alcohol consumption. Human Papilloma Virus (HPV) infection, asbestos exposure and irradiation have also shown increased incidence. Males are affected more than females. It most frequently presents in the 6th decade of life.Laryngeal cancer may spread by invading into surrounding structures, via lymphatics usually to local cervical nodes or haematogenous metastasis most commonly to the lungs. Common symptoms on presentation include dysphonia, dysphagia, odynophagia, globus and cough. Less commonly haemoptysis, stridor, dyspnoea and halitosis may be described. Treatment varies on the stage of the disease. Smoking and alcohol cessation are important for all disease stages. In early disease laryngeal preservation treatments may include laser therapy, microsurgery and radiotherapy. Later stage disease treatments may involve a combination of laryngectomy, radiotherapy and chemotherapy.

Clinical HistoryA 37-year old male patient presents with a 1-month history of lethargy, cough and weight loss. He had a history of an orchiectomy 18 months previous for a testicular tumour. Then 12 months post-op he underwent neck radiotherapy to treat metastasis. On admission, he became acutely dyspnoeic and hypoxic and died.Pathology This right lung specimen (and portions of 4 ribs) has been sliced longitudinally. There are numerous rounded tumour nodules evident in the lung parenchyma ranging from 5 to 30mm in diameter. The tumours are variegated in appearance with pale yellow and dark brown cut surfaces. One tumour is extending along the bronchus of the lower lobe forming a cast. Several nodules project from the pleural surface and some show central umbilication from necrosis and haemorrhage. This is an example of pulmonary metastases from a mixed germ cell testicular tumour, most likely choriocarcinoma arising in a malignant teratoma.Further InformationGerm cell testicular tumours (GCT) are the most common tumours found in men. Average age of diagnosis is 30 year of age and are rarely diagnosed pre-puberty. Risk factors for development include cryptorchidism and a positive family history of GCT. Familial GCT increased risk can be linked to genes encoding for kinases, e.g. KIT and BAK.They can be divided into two groups: seminomatous (resemble primordial germ cells) and non-seminomatous (resemble embryonic stem cells). Over one third of GCT are mixed GCT, with two or more GCT types in one mass. Many possible combinations of seminoma, teratoma, embryonal carcinoma, yolk sac tumor, and choriocarcinoma can be seen. Teratomas components are found in one third of mixed GCT. Elevated serum Alpha Fetoprotein and beta-hCG are produced by choriocarcinoma. Lymphatic spread involves the retroperitoneal para aortic nodes initially. Mediastinal and supraclavicular nodes may later become involved. The lungs are the most common site for haematogenous spread but the liver, brain or bones may also be affected.Symptoms may include a painless testicular mass and haematospermia. Later symptoms of distant metastases may occur. Common symptoms of lung metastases include cough, dyspnoea, haemoptysis, recurrent infectionTreatment depends on clinical stage but usually involves radical orchiectomy, chemotherapy and sometimes radiotherapy. More than 95% on early stage GCT can be cured.

Clinical HistoryThere is no clinical history for this specimen.PathologyThe specimen is a parasagittal section of the left lung. There are patchy regions of focal consolidations and discolorations caused by congested and hyperaemic lung tissue distributed within both lobes; however, the upper lobe is more severely affected. The consolidation appears to be concentrated around the bronchioles, which are ectatic. The costal (pleural) surface of the upper lobe is especially discoloured.Further InformationBronchopneumonia is a form of pneumonia characterized by inflammatory exudate within the intra-alveolar space resulting in consolidation that affects a large and continuous area of the lobe of a lung. It is one of the two anatomic classifications of pneumonia (the other being lobar pneumonia). The affected regions in this case shows classical focal red hepatization or consolidation in focal regions, which is due to vascular congestion with extravasation of red cells into alveolar spaces, along with increased numbers of neutrophils and fibrin. The filling of airspaces by the exudate leads to a gross appearance of solidification, or consolidation, of the alveolar parenchyma.Bronchopneumonia is a subtype of pneumonia. It is the acute inflammation of the bronchi, accompanied by inflamed patches in the peribronchial and peribronchiolar lobules of the lungs.It is often contrasted with lobar pneumonia but in clinical practice the types are difficult to apply, as the patterns usually overlap. Bronchopneumonia (sometimes called lobular) often leads to lobar pneumonia as the infection progresses to affect an entire lobe. The same organism may cause one type of pneumonia in one patient, and another in a different patient. CausesBronchopneumonia is usually a bacterial pneumonia rather than being caused by viral disease and is more commonly a hospital-acquired pneumonia than a community-acquired pneumonia, in contrast to lobar pneumonia.

Clinical HistoryA 74-year old male presented with increasing shortness of breath and haemoptysis. Further history reveals 20kg weight loss in 6 months, night sweats and a chronic cough. He has recently moved from a country where TB is endemic. On examination, he has hypoxic and tachypnoea and has bilateral crepitations throughout his lung fields and a dull left lung base on percussion. His quantiferon gold blood test is positive. His chest x-ray showed bilateral small nodular deposits and a left basal pneumonia. He died from respiratory failure soon after admission.PathologyThe right lung has been sliced longitudinally and mounted to display the cut surface. The bronchi and bronchioles are mildly ectatic. Scattered throughout the entire lung parenchyma are large numbers of small, pale yellows nodules less than 1 mm in diameter. Similar tiny subpleural nodules are seen on the surface of the visceral pleura. The nodules are tubercles. This is miliary tuberculosis, so-called due to the resemblance of the nodules to millet seeds.Further InformationTuberculosis (TB) is a chronic pulmonary and systemic infectious disease caused by Mycobacterium tuberculosis. Transmission most commonly occurs via inhalation of aerosolized droplets of this pathogenic bacteria, first described by Robert Koch (1882). Risk factors for contracting TB include being an inhabitant of a developing country where the disease is endemic, immunosuppression (e.g. HIV, steroid use, anti-TNF use and diabetes), chronic lung disease (e.g. silicosis), alcoholism and malnutrition.After initial pulmonary infection of M. tuberculosis clinical manifestation varies. In 90% of individuals with an intact immune system they enter an asymptomatic latent infection phase. This latent TB may reactivate at any time in the patient‘s life. In the other 10% of patients, especially in the immunocompromised, they develop primary disease which is immediate active TB infection. Manifestations of primary TB include pulmonary infection symptoms (e.g. consolidation, effusion and hilar adenopathy) and extra pulmonary symptoms including lymphadenopathy, meningitis and disseminated miliary TB.Secondary tuberculosis occurs when there is reactivation of previous latent TB infection. Around 10% of latent TB will reactivate usually during periods of weakened host immunity. Typical symptoms of reactivation are cough, haemoptysis, low grade fever, night sweats and weight loss.Miliary TB occurs when the mycobacterium erodes into a pulmonary vein and seeds elsewhere. The organism can circulate back to the lung and disseminate thought the lung parenchyma as in this case. Systemic miliary tuberculosis can occur when the mycobacterium is disseminated through the arterial system. The TB can then deposit in any organ but most commonly in the liver, bone marrow, spleen and adrenal glands.The immune response against TB is mediated via TH1 cells stimulate alveolar macrophages to attack the mycobacteria. These macrophages surround the infection forming a granuloma surrounding a central area of ‘caseous’ (white cheese-like) necrosis. Secondary pulmonary TB may heal with fibrosis or progress as in this case. Progressive pulmonary TB sees erosion and expansion of the infectious lesion into adjacent lung parenchyma. This leads to evacuation of the caseous centre leading to fibrous cavitation. Erosion of blood vessels can occur causing haemoptysis. Post treatment of TB the tissue heals by fibrosis but does not recover the pulmonary architecture.TB diagnosis is usually made with a clinical history and chest x-ray and multiple sputum cultures. Mantoux skin tuberculin test and serum interferon gamma release assay may also be used to help screen for infection. Biopsies may be taken of suspected infection site for culture to assist diagnosis. Treatment involves prolonged courses of multiple antibiotics, which depend on the antibiotic resistance of the infecting mycobacterium.

Clinical HistoryThere is no clinical history for this specimen.Pathology The specimen is a parasagittal section of the right lung and the boundaries between the upper and lower lobes is clearly visible. The entire upper lobe is congested and pale grey in colour.Further InformationThis is an example of a stage of lobar pneumonia in which the inflammatory exudates within the intra-alveolar space resulting in consolidation that affects a large and continuous area of the lobe of a lung. The affected lobe in this case shows grey hepatisation or late consolidation. This usually occurs 2 to 3 days following red hepatisation, and lasts for 4 to 8 days. The lung appears grey with liver-like solid consistency, due to a fibrinopurulent exudate, progressive disintegration of red blood cells, and haemosiderin. Large numbers of macrophages begin to appear in the interstitial tissue. They are the dominant cells, which attempt to clear away the cellular debris and acute inflammation through phagocytosis. The macrophages may contain iron due to consumption of erythrocytes, and are thus termed siderophages. Following grey hepatisation, resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally, which liquefies the previous solid fibrinous content and eventually restores aeration.The most common organisms that cause lobar pneumonia are Streptococcus pneumoniae, also called pneumococcus, Haemophilus influenzae and Moraxella catarrhalis. Mycobacterium tuberculosis, the tubercle bacillus, may also cause lobar pneumonia if pulmonary tuberculosis is not treated promptly. Other organisms causing lobar pneumonia are Legionella pneumophila and Klebsiella pneumoniae.[2]On a posterioanterior and lateral chest radiograph, an entire lobe will be radiopaque, which is indicative of lobar pneumonia.

Clinical HistoryA 6-year old girl was admitted with a productive cough, dyspnoea and fevers. She became increasingly hypotensive and dies soon after admission. She had a previous history of recurrent pneumonia and meconium ileus. The clinical diagnosis was cystic fibrosis (mucoviscoidosis). Her sister died aged 3 from the same disease.Pathology The lung parenchyma shows extensive changes mainly with a bronchial distribution. Many bronchi are dilated (bronchiectasis) and contain thick, yellowish, purulent material. These changes are most marked in the upper lobe, at the apex of which a small focus of ‘honeycomb’ change is also seen. Multiple abscesses are present, especially in the basal and central parts of the lower lobe. The base of the lower lobe is severely affected with fibrosis and consolidation being evident. There is very little normal lung tissue remaining. These pathological changes are characteristic but not pathognomonic of cystic fibrosis.Further InformationCystic fibrosis (CF) is an inherited disorder of chloride ion transport. Mutations in the cystic fibrosis conductance regulator (CFTR) gene on chromosome 7 cause defects in the chloride channel protein leading to dysfunction of the chloride channels. This causes increased water absorption in exocrine glands and epithelium of the respiratory, gastrointestinal and reproductive tracts. These dehydrated viscous secretions then obstruct these organ passage causing clinical features including: persistent pulmonary infection, pancreatic insufficiency, liver cirrhosis, intestinal obstruction, male infertility, and elevated sweat chloride levels. In the airway, CF patients have decreased chloride secretion and increased water reabsorption. This causes dehydrated mucous lining the airways leading to defective mucociliary action, mucous obstructing the airway, bronchiole dilatation (bronchiectasis) and secondary infection. Staphylococcus aureus, Haemophilus influenzae and Pseudomonas are the most common bacteria causing CF patients’ lower respiratory tract infections. Chronic bronchitis and bronchiectasis develops as a result. Pulmonary issues are the highest cause of mortality in CF patients. The average life expectancy is between 40-50 years of age in developed countries.CF occurs in around 1 in 3000 live births. It is inherited in an autosomal recessive pattern. It is most common in fair-skinned populations: with 1 in 20 being a carrier of the gene. Symptoms can present in-utero or even up to adolescence, depending on the severity of the disease. It is now most commonly diagnosed with the neonatal screening test for immunoreactive trypsinogen (a pancreas enzyme precursor). If this screening test is positive, a formal diagnosis is made with a sweat test showing >60mmol/L of chloride.

Clinical HistoryThis 47-year old woman was admitted with terminal carcinomatosis. On examination, a hard liver and a right pelvic mass were palpable. She had been ill with constitutional symptoms for months and she finally sought medical attention. She was admitted for palliative care and died shortly afterwards.PathologyThe left intact lung has multiple pale tumour nodules of varying size are scattered throughout the lung substance. Near the hilum several nodules are confluent. The hilar lymph nodes contain pale tumour tissue. Small tumour nodules from 2mm to 2cm can be seen beneath the thickened pleura on the costal, mediastinal and diaphragmatic surfaces. Histologically, these were metastatic deposits of adenocarcinoma. At post-mortem there was an adeno-carcinoma of ovary, with metastases in lungs, heart, liver and pericardium.Further informationPulmonary metastases are more common than primary lung cancer. Malignant diseases arising anywhere in the body may spread to the lungs due to its rich blood supply and lymphatic drainage. Sarcomas usually metastasize by the bloodstream, and carcinomas spread either via the bloodstream or the lymphatic system or both.

Clinical HistoryA 74-year old male presented with a 2-months history of dysphagia, dysphonia and weight loss. He had a history of heavy alcohol consumption and smoked 40 cigarettes per day for 40 years. Investigation discovered a laryngeal tumour. He received radiotherapy but his tumour reoccurred. He died 9 months after his initial presentation.PathologyThe specimen consists of tongue, pharynx, larynx, oesophagus and trachea and has been mounted in the coronal plane. The oesophagus and trachea have been opened from the posterior aspect. There is a 5 x 4 x 2 cm fungating carcinoma evident extending into both pyriform fossae. The surface of the tumour is irregular with shaggy areas of necrosis. The tumour has arisen from the larynx and involves both vocal cords, the left aryepiglottic fold and both pyriform fossae.Further InformationOver 95% of laryngeal cancers are squamous cell carcinomas. The tumour usually develops on the vocal cords but may occur above or below the cords, on the epiglottis, aryepiglottic folds or in the pyriform fossae. The cancer usually begins as squamous cell carcinoma in situ, progressing to ulcerated and fungating invasive carcinoma with continued exposure to carcinogens. The greatest risk factors for developing cancer of the larynx are tobacco smoke and alcohol consumption. Human Papilloma Virus (HPV) infection, asbestos exposure and irradiation have also been shown to be associated with increased incidence of head-and-neck squamous cell carcinoma (HNSCC). Males are affected more than females. It most frequently presents in the 6th decade of life. Laryngeal cancer may spread by invading into surrounding structures, via lymphatics usually to local cervical nodes, or haematogenous metastasis most commonly to the lungs. Common symptoms of HNSCC on presentation include dysphonia, dysphagia, odynophagia, globus and cough. Less commonly haemoptysis, stridor, dyspnoea and halitosis may be described.Treatment varies on the stage of the disease. Smoking and alcohol cessation are important for all disease stages. In early disease laryngeal preservation treatments may include laser therapy, microsurgery and radiotherapy. Later stage disease treatments may involve a combination of laryngectomy, radiotherapy and chemotherapy.HPV-related HNSCC have better outcomes than those non-HPV positive tumours. HPV-vaccination programmes have been introduced in several countries, including Australia and the UK, for both boys and girls, in order to reduce their risk for HNSCC.

Clinical HistoryA 60-year old male presents with a 6-week history of globus (i.e. the feeling of a lump in his throat) and dysphonia. On examination, he had enlarged cervical lymph nodes. Investigations discovered a laryngeal tumour. He underwent a laryngectomy and a cervical lymph node dissection. He made a full recovery.Pathology The specimen is the amputated larynx viewed from behind. It shows an irregular fungating tumour arising from the left pyriform fossa. There is distortion and oedema of the laryngeal tissues. Histologically, this was a squamous cell carcinoma.Further InformationOver 95% of laryngeal cancers are squamous cell carcinomas (SCC). The tumour usually develops on the vocal cords but may occur above or below the cords, on the epiglottis, aryepiglottic folds or in the pyriform sinuses. The cancer usually begins as carcinoma in situ, progressing to ulcerated, fungating invasive carcinoma with continued exposure to carcinogens.The greatest risk factors for developing cancer of the larynx are tobacco smoke and alcohol consumption. Human Papilloma Virus (HPV) infection, asbestos exposure and irradiation have also shown increased incidence. Males are affected more than females. It most frequently presents in the 6th decade of life. Laryngeal cancer may spread by invading into surrounding structures, via lymphatics usually to local cervical nodes or haematogenous metastasis most commonly to the lungs. Common symptoms on presentation include dysphonia, dysphagia, odynophagia, globus and cough. Less commonly haemoptysis, stridor, dyspnoea and halitosis may be described. Treatment varies on the stage of the disease. Smoking and alcohol cessation are important for all disease stages.In early disease laryngeal preservation treatments may include laser therapy, microsurgery and radiotherapy. Later stage disease treatments may involve a combination of laryngectomy, radiotherapy and chemotherapy. HPV-related HNSCC have better outcomes than those non-HPV positive tumours. HPV-vaccination programmes have been introduced in several countries, including Australia and the UK, for both boys and girls, in order to reduce their risk for HNSCC.

Clinical HistoryA 57-year old male presented with a 3-week history of cough and pleuritic left sided chest pain. Chest x-ray showed left upper lobe collapse with large left sided pleural effusion. Pleurodesis aspirated frank pus from the pleural cavity. He later died despite pleural drainage and antibiotic treatment.Pathology This specimen shows the lower trachea and main bronchi. These have been cut open and the left upper lobe has been sliced to display the cut surface. At the point of origin of the left upper lobe bronchus there is an impacted foreign body; an inhaled rabbit vertebra! As a result of the obstruction, the upper lobe has collapsed, pneumonia has developed and the pleural surface is covered by fibrinous exudate. This is an inhaled foreign body with associated collapse and pneumonic consolidation of the left upper lobe and empyema.Further InformationInhalation of a foreign body or foreign body aspiration (FBA) occurs when a foreign body is inhaled into the airway causing partial or complete obstruction of the airway. This can potentially be fatal. It is more common in children than adults. It is a leading cause of accidental death worldwide. FBA poses greatest risk of death to those less than 1-year old and patients over 75 years of age.Risk factors for FBA in adults include decreased level of consciousness, drug or alcohol intoxication, or anaesthesia. In the elderly additional risk factors include medication use (impairing cough and swallowing), stroke-related dysphagia, and degenerative neurologic diseases, such as Alzheimer‘s or Parkinson‘s disease. In adults, the most commonly aspirated foreign bodies include inorganic items (e.g. nails, pins, dental debris) and organic material (e.g. bones, improperly chewed meat, and watermelon seeds). Symptoms on presentation vary depending on the degree of airway obstruction caused. Larger obstruction may present as choking or sudden asphyxia. Smaller foreign bodies may present with more insidious symptoms such as cough, dyspnoea, fevers, chest pain and haemoptysis. Airway collapse distal to the foreign body will lead to infection. Treatment involves retrieval of the foreign body with bronchoscopy or emergency tracheostomy.

Clinical HistoryA 89-year old male presents with an episode of large haemoptysis. He has a history of diabetes and immunosuppression secondary to steroid treatment for rheumatoid arthritis. Further history reveals a long history of cough, haemoptysis, fevers and weight loss. On examination, he is noted to be cachexic, hypoxic and have crepitations throughout the left lung. Chest x-ray shows multiple cavitation lesions in the left lung. Subsequently, he has another massive haemoptysis and dies.PathologyThe left lung is cut longitudinally to display the cut surface. The upper lobe is almost entirely replaced by several large irregular cavities lined by necrotic debris and fibrous tissue. Blood vessels are seen in the upper cavity with evidence of haemorrhage. The lower lobe contains several smaller caseous areas, some of which are breaking down. The intervening lung parenchyma is scarred. The pleura is thickened. This is fibrocaseous tuberculosis with cavitation.Further InformationTuberculosis (TB) is a chronic pulmonary and systemic infectious disease caused by Mycobacteria tuberculosis. Transmission most commonly occurs via inhalation of aerosolized droplets of M. tuberculosis. Risk factors for contracting TB include being an inhabitant of a developing country where the disease may be endemic, immunosuppression (e.g. HIV, steroid use, anti-TNF use and diabetes), chronic lung disease (e.g. silicosis), alcoholism and malnutrition.After initial pulmonary infection of M. tuberculosis clinical manifestation varies. In 90% of individuals with an intact immune system they enter an asymptomatic latent infection phase. This latent TB may reactivate at any time in the patient‘s life. In the other 10% of patients, especially in the immunocompromised, they develop primary disease which is immediate active TB infection. Manifestations of primary TB include pulmonary infection symptoms (e.g. consolidation, effusion and hilar adenopathy) and extra pulmonary symptoms including lymphadenopathy, meningitis and disseminated miliary TB.Secondary tuberculosis occurs when there is reactivation of previous latent TB infection. Around 10% of latent TB will reactivate usually during periods of weakened host immunity. Typical symptoms of reactivation are cough, haemoptysis, low grade fever, night sweats and weight loss.The immune response against TB is mediated via TH1-cells stimulate alveolar macrophages to attack the mycobacteria. These macrophages surround the infection forming a ‘granuloma’ with central caseous necrosis.Secondary pulmonary TB may heal with fibrosis or progress as in this case. Progressive pulmonary TB sees erosion and expansion of the infectious lesion into adjacent lung parenchyma. This leads to evacuation of the caseous centre leading to fibrous cavitation. Erosion of blood vessels can occur causing haemoptysis. Post treatment of TB the tissue heals by fibrosis but does not recover the pulmonary architecture.TB diagnosis is usually made with a clinical history and chest x-ray and multiple sputum cultures. Mantoux skin tuberculin test and serum interferon gamma release assay may also be used to help screen for infection. Biopsies may be taken of suspected infection site for culture to assist diagnosis. Treatment involves prolonged courses of multiple antibiotics, which depend on the antibiotic resistance of the infecting mycobacterium.

Clinical HistoryThere is no clinical history for this specimen.Pathology The specimen is a parasagittal section of the right lung and the boundaries between the three lobes are visible. The entire upper and middle lobes are congested and hyperaemic* causing the darker appearance. There are smaller foci in the left lung.Further InformationLobar pneumonia is a form of pneumonia characterized by inflammatory exudate within the intra-alveolar space resulting in consolidation that affects a large and continuous area of the lobe of a lung. It is one of the two anatomic classifications of pneumonia (the other being bronchopneumonia). The affected lobe in this case shows classical red ‘hepatization’ or consolidation of the lung parenchyma, which is due to vascular congestion with extravasation of red cells into alveolar spaces, along with increased numbers of neutrophils and fibrin. The filling of the airspaces by the exudate leads to a gross appearance of solidification, or consolidation, of the alveolar parenchyma. This reddish appearance has been likened to that of cut surface of the liver, hence the term "hepatization".The most common organisms that cause lobar pneumonia are Streptococcus pneumoniae, also called pneumococcus, Haemophilus influenzae and Moraxella catarrhalis. Mycobacterium tuberculosis, the tubercle bacillus, may also cause lobar pneumonia if pulmonary tuberculosis is not treated promptly. Other organisms that lead to lobar pneumonia are Legionella pneumophila and Klebsiella pneumoniae.Like other types of pneumonia, lobar pneumonia can present as a community-acquired infection, in immune suppressed patients or as nosocomial infection. However, most causative organisms are of the community-acquired type.On a posteroanterior and lateral chest radiograph, an entire lobe will be radiopaque with no evidence of air within it, indicative of lobar pneumonia.*Hyperaemia = active engorgement of vascular beds with a normal or decreased outflow of blood.

Clinical HistoryA 32-year-old female G3P0 (gravida 3, para 0‘ – i.e., has had two pregnancies, with neither of the embyros surviving to a gestational age of 24 weeks) presents in preterm labour at 25 weeks gestation. The GP had noted an increased fundal height at 30cm one week prior, but the mother had refused prenatal testing or ultrasound, and was lost to follow up. She delivered a live born male baby. Examination of the baby noted polydactyly, imperforate anus, excessive drooling, and a loud pan-systolic murmur. A single umbilical artery was noted in the umbilical cord. The baby had difficulty feeding with increasing respiratory distress. The baby died 2 days later from aspiration pneumonia.Pathology/Specimen DetailsThe specimen comprises the tongue, larynx, trachea, bronchi, both lungs and oesophagus of the foetus. The trachea and bronchi have been divided in the midline. A fistula is present just above the bifurcation at a communicating fistula can be seen connecting the distal oesophagus to the trachea (arrow). This is an example of a Type C Tracheoesophageal Fistula (oesophageal atresia with distal tracheoesophageal fistula). It is difficult to discern if the oesophagus ends as a blind pouch at the lower extent of the specimen.Further InformationTracheoesophageal Fistula (TEF) is a common congenital abnormality occurring in about 1 in 4000 live births. TEF usually occurs with oesophageal atresia (sometimes abbreviated to EA, reflecting the US spelling of ‘esophagus’). TEF are classified according to their anatomical configuration. Type C is the most common configuration; as described above, in which oesophageal atresia with distal tracheoesophageal fistula making up 86% of cases. TEF occurs without oesophageal atresia in only 4% of cases, Type E.TEF and oesophageal atresia are caused by defective lateral septation of the foregut into the oesophagus and trachea. It is believed that a defect in epithelial-mesenchymal interactions causes failed branching of a lung bud branch which becomes the fistula tract. It is associated with VACTERL (vertebral defects, anal atresia, cardiac defects, TEF, renal anomalies, and limb abnormalities) or CHARGE syndrome (Coloboma, Heart defects, Atresia choanae, Growth retardation, Genital abnormalities, and Ear abnormalities).Oesophageal atresia can be seen on prenatal ultrasound as polyhydramnios, absent/collapsed stomach, and proximal oesophageal pouch dilation. EA with TEF can be more difficult to see on ultrasound as fistula allows fluid flow into the stomach. Polyhydramnios occurs in one third of cases of EA with distal TEF. Postnatal symptoms vary on the configuration of the fistula. These include excessive drooling, respiratory distress, difficulty feeding and choking. Reflux of gastric contents can lead to aspiration pneumonia as in this case.Diagnosis can be made by failing to pass a nasogastric tube into the stomach along with X-ray imaging. Fluoroscopy with contrast can be used for more indeterminate cases. For milder cases diagnosis may be made later with endoscopic investigation. Treatment involves surgical correction of the defects. Prognosis is usually good. However, cases with associated chromosomal, prematurity and cardiac defects are at increased risk of death.

Clinical HistoryA 45-year old male presented with a lump in his left supraclavicular area. The swelling had been increasing in size over 6 months. Excision biopsy of the lump showed Hodgkin lymphoma (HL). Ten months later he was readmitted with left shoulder pain and swelling of his left arm. Examination revealed generalised lymphadenopathy with significant swelling in his left supraclavicular and axillary regions. He was treated with radiotherapy and Thiotepa chemotherapy. He developed vomiting. A subsequent barium meal showed duodenal obstruction from extrinsic lymph node compression. He continued to deteriorate and died 2 weeks after readmission.Pathology The 3D print shows the tracheal bifurcation with adjacent para-tracheal and peri-bronchial lymph nodes. The trachea has been opened longitudinally and is viewed from behind. The para-tracheal lymph nodes are pale and matted (fused) together. Similar abnormal tissue is seen as a confluent pale mass on the left side of the trachea, above the aortic arch, which is seen cut in cross-section as a void space with branches arising. The peri-bronchial lymph nodes are also enlarged, and contain carbon pigment. The circumscribed small paler areas in the lymph nodes and extra-nodal tumour are foci of necrosis. There is an atheroma in the wall of the aorta but it is difficult to see in the 3D print.Further InformationHodgkin Lymphoma (HL) is a malignancy of lymphocytes. It is characterised by the presence of neoplastic giant cells called Reed Sternberg cells. There are 5 main subtypes according to the WHO Lymphoma Classification, based on the morphology, immunophenotyping and genetics. Activation of the transcription factor NF-kB is a common pathway of tumorigenesis among the subtypes. This promotes proliferation, reduces apoptosis, and induces expression of cytokines that recruit the immune cells that surround Reed Sternberg cells in HL.There is a bimodal age distribution with a peak in late adolescence/early adulthood and a second peak in older adults. HL accounts for just under 1% of all cancers worldwide. Infection with Epstein Barr Virus (EBV) contributes to the pathogenesis of the main subtypes of HL. The viral genome causes genetic alterations that lead to aberrant signal pathways, although the precise mechanism is not known. Immunosuppression (e.g. HIV infection or post- organ transplant) and positive HL family history are also risk factors. HL commonly presents as painless lymphadenopathy, pruritus, weight loss, fevers and night sweats. Later disease sees organ spread to the spleen, liver and bone marrow. Compressive symptoms can arise from enlargement of lymph nodes and infiltrated organs. HL is diagnosed with staging CT scan, excision biopsy of involved nodes and bone marrow biopsy. Treatment involves radiotherapy and chemotherapy. Although previously incurable, the overall survival of HL has improved significantly over the last 5 decades as a result of modern therapies: diagnosed at an early stage, it is almost 90%, and even later stage disease has a favourable prognosis.

Clinical HistoryA 55-year old female presents with severe dyspnoea, a productive cough and oral candidiasis. She is immunosuppressed with a history of rheumatoid arthritis being treated with steroids and cyclophosphamide. Sputum cultures grew staphylococcus aureus. She was commenced on appropriate therapy but died shortly after admission.Pathology The right lung has been bisected. There are multiple irregular abscess cavities visible. The largest of these, in the apex of the lower lobe, measures 4 x 3 cm in diameter. At the apex of the upper lobe, there is another irregular abscess cavity which is less obvious, approximately 3 x 2 cm in diameter surrounded by a zone of consolidation. A number of small abscesses are also seen. Patchy consolidation is present in the middle lobe. Numerous bronchi contain and are obstructed by plugs of pus. Cultures taken from the specimen grew Staph. aureus. This is an example of multiple Staphylococcal lung abscesses in an immunosuppressed patient.Further InformationStaphylococcus aureus is a gram-positive coccus. It is part of the microbiota of the human body usually found on the skin or upper respiratory tract. It is usually commensal but may cause opportunistic infections such as skin infections commonly or less frequently, pneumonia and endocarditis. It can cause both community and hospital-acquired pneumonia. Hospital-acquired Staph pneumonia is most commonly associated with intubation and prolonged admissions. Prevalence of hospital acquired pneumonia caused by Methicillin-Resistant Staph Aureus (MRSA) is increasing.It is an important cause of secondary bacterial pneumonia in patients following viral respiratory infection e.g. post influenza infection. Intravenous drug users have an increased risk of developing ‘metastatic’ Staph. aureus pneumonia and endocarditis, as a result of staph bacteraemia caused by the use of dirty needles. Staph. aureus pneumonia is severe and associated with an increased rate of complications, such as ca vitating abscess formation and empyema.Staph Aureus pneumonia should be suspected in any of the high-risk groups above as well as patients with pneumonia with rapid deterioration, haemoptysis, early multilobar pneumonia on X-ray, pulmonary cavitation or disseminated intravascular coagulation. First line treatment for Staph. aureus pneumonia is penicillin antibiotics, such as flucloxacillin. Staph aureus resistance to penicillin is very common with penicillinase production e.g MRSA. MRSA is treated with glycopeptide antibiotics, such as vancomycin, or oxazolidinone antibiotics, such as linezolid.