PULMONARY PATHOLOGY FOR FORENSIC PATHOLOGISTS. David Moffat Pathology Update 2019

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PULMONARY PATHOLOGY FOR FORENSIC PATHOLOGISTS David Moffat Pathology Update 2019

This session will be in the form of a slide seminar, reflecting 12 years of referral practice from forensic autopsies. The cases will be representative of those submitted for opinion and will encompass a spectrum of neoplastic and non-neoplastic conditions (mesothelioma has been specifically excluded). Digital slides will be made available to delegates for viewing before the meeting. https://virtual.rcpaqap.com.au/uniview/#/apilaunch?pat_id=201 9DAVIDMOFFAT&mrn_integration_id=14B41E16-1ED0-4AA6-84AA- EB44274285FB&uniview_cmd=show_images&allow_pat_chan ge=0&limited_access=1

Case 1 78 year old male. Admitted to hospital following infective exacerbation of COPD. Died after drug administration error. Known history of right lung lower lobe mass. Background lung appears extremely abnormal. What is the possible relevance to the cause of death?

Haemosiderosis Endogenous pneumoconiosis Encrustation of elastic laminae of blood vessels and alveolar wall by haemosiderin and calcium Foreign body giant cell reaction Haemosiderin laden intra-alveolar macrophages Perl s stain stronger than in smokers macrophages Mild interstitial fibrosis and type II pneumocyte hyperplasia +/- capillaritis

Causes of haemosiderosis Localised causes (TB; tumours; infarction) Generalised bleeding disorders Pulmonary hypertension Occlusion of pulmonary veins Mitral stenosis Atrial myxoma Mediastinal fibrosis Veno-occlusive disease Lymphangioleiomyomatosis Capillary haemangiomatosis Vasculitis (ANCA-related; Goodpasture s syndrome; immune complex mediated) pulmonary-renal syndrome Chemical injury Asphyxia Idiopathic (children & young adults)

Case 3 60 year old female. Collapsed after acute shortness of breath. An echocardiogram on admission to hospital showed large right ventricle. She had pericardial and bilateral pleural effusions, pitting oedema and was hyponatraemic. A diagnosis of pulmonary hypertension and cor pulmonale was made. Care was withdrawn after an MRI showed hypoxic ischaemic encephalopathy. Medical history of hepatitis C infection, COPD, squamous carcinoma of mouth, right middle lobectomy for extralobar pulmonary sequestration and talc pleurodesis.

Filler embolism IVDA lung Usually starch, talc or cellulose May cause pulmonary hypertension Post mortem examination of heart confirmed right ventricular hypertrophy Histology of liver: refractile material also in portal tracts

Causes of pulmonary hypertension Precapillary Constrictive Primary pulmonary hypertension Congenital heart disease Liver disease HIV (antiretroviral drugs) Appetite suppressing drugs Hereditary haemorrhagic telangiectasia Connective tissue disease Hypoxic High altitude living COPD Sleep apnoea Embolic Thromboembolic Parasitic Foreign material Capillary Pulmonary fibrosis Capillary haemangiomatosis Diffuse smooth muscle proliferation Postcapillary Left sided heart disease Veno-occlusive disease

Histology of pulmonary hypertension Medial hypertrophy No muscle in vessels <30 μm diameter Muscle on one side only in vessels 30-100 μm Intimal fibrosis Concentric Eccentric (thromboembolic) Longitudinal smooth muscle in intima (hypoxic) Plexogenic arteriopathy (only in constrictive precapillary causes) Fibrinoid necrosis Dilatation lesions Haemosiderosis

Definition of right ventricular hypertrophy Right ventricular weight > 80g Ratio of weight of left ventricle plus septum to right ventricle < 2:1

Intravascular talcosis Nine cases of histologically confirmed intravascular talcosis Including five autopsy cases Two patients denied history of intravenous drug use

Case 2 77 year old female. Died from multiple injuries following a road traffic accident. Medical history of asthma, atrial fibrillation, anaemia, hypertension and dilated cardiomyopathy. Do the changes in the lung represent a reactive phenomenon or in situ malignancy?

Lambertosis Non-specific effect of chronic brochiolitis Results in bronchiolisation (peribronchiolar metaplasia) of adjacent alveolar spaces Possible causes include respiratory bronchiolitis and hypersensitivity pneumonitis Can mimic lepidic pattern adenocarcinoma or atypical adenomatous hyperplasia

Case 9 77 year old female. Died following sudden collapse and respiratory arrest.

Diffuse alveolar damage Mortality 70% Interstitium expanded by fibroblasts and inflammatory cells Hyperplasia and atypia of type II pneumocytes Squamous metaplasia Thrombi

DAD Exudative phase: hyaline membranes Organising/proliferative phase: organising pneumonia (COP is more patchy and peribronchial) NSIP-like pattern if survives

DAD Causes: Infection (especially viral) Inhalation of smoke, toxic gases, high concentration oxygen Aspiration of gastric contents Irradiation Shock, including sepsis Reperfusion injury Cardiopulmonary bypass Acute pancreatitis Fat embolism Paraquat poisoning Chemotherapy Idiopathic (acute interstitial pneumonia, acute exacerbation of UIP)

Case 4 81 year old male. Bangladeshi origin, living in USA. Died 5 days after arrival in Australia following a visit to Bangladesh for several weeks. Complained of shortness of breath and haemoptysis for 2 days prior to being found dead in bed. Medical history of COPD, asthma and previous pulmonary thromboembolism. At autopsy fresh and altered blood seen around mouth, in larynx, trachea and bronchi; right lung markedly haemorrhagic; small amount of altered blood in oesophagus and stomach

Active secondary tuberculosis Likely to have caused fatal pulmonary haemorrhage

Case 8 42 year old female. Died of mixed drug toxicity. Medical history of bipolar affective disorder, epilepsy, asthma and pancreatitis.