GROSS DICTATION TEMPLATES

The patient expired on ____ at __: __am and permission for complete autopsy is given by the WIFE, Mrs. ___ on _/_/_. The autopsy was performed on _/_/_at __: __am. The body is that of a well-developed, well-nourished man weighing approximately __ lb. and measuring __ inches in length, appearing around the recorded age of __years. Liver mortis is slight and unfixed. Rigor mortis is slight and limited to the distal extremities. The hair is not present. Irides are brown. The pupils are equal and round and bilaterally dilated. The sclerae are not jaundiced. The ears and nose are symmetric. The teeth are present. The buccal mucosa is pink. The neck is supple, and trachea is midline. Cervical veins are not distended. The chest is symmetric. The abdomen is soft and obese with multiple thick, white vertical striae. The liver edge and spleen tip are not palpable. There is no pedal edema. The external genitalia are unremarkable. There is a __cm ecchymosis on right inguinal region. The spine appears straight. The extremities are symmetric and well developed. The digits and palmar markings appear unremarkable. There is no clubbing. The skin color is tan with single tattoo and several scars, including tattoo on right arm, and scars on right and left knee (measuring __ cm each), Saphenous vein graft scar on left thigh and leg (measuring __ cm), scar on left forearm (__cm) scar on left wrist (__cm), midline scar on chest (__cm). The following medical paraphernalia are in place: Hospital ID bracelet/tag – right wrist and toe PICC line Intravenous catheter INTERNAL EXAMINATION: The body is opened with a Y-incision. The panniculus adiposus measures 4.6 cm at the umbilicus. There is 80-100ml of clear, yellow-pink serosanguinous peritoneal fluid. The pleural surfaces are glistening and smooth with few lateral adhesions. There is a moderate amount of pleural fluid. The right hemithorax contains 260 ml of blood tinged, serosanguineous fluid; the left contains 180 ml of blood tinged, serosanguineous fluid. Pulmonary arteries are examined with no obvious evidence of pulmonary emboli. The mediastinum is midline. The pericardial sac is open and reveals 50 ml of clear, blood (hemopericardium). CARDIOVASCULAR SYSTEM: The heart is large and weighs 680 grams. The superior and inferior caval veins connect with the right atrium. The tricuspid, pulmonic, mitral, and aortic valves measure 10.5, 6.5, 7, 6 cm respectively. The right and left ventricular chamber are moderately dilated, and its walls average 1.0 cm and 1.5 cm in thickness respectively. There is a moderate amount of epicardial fat. The epicardial surface is smooth with adhesions with pleura. The foramen ovale is non-patent. There are no thrombi in the auricular appendages. The valve leaflets and cusps are mildly thickened. The mitral valve is moderately thickened and calcified. The chordae tendineae are slightly thickened. The endocardial surfaces are smooth. The myocardium is red-brown and shows a recent infarct in the posterolateral wall of left ventricle. The interarterial and interventricular septums are intact. The coronary ostia are patent. The coronary arteries course in the usual fashion and are patent with severe calicifications. They are serially sectioned to reveal plaques or calcifications. No vegetations are appreciated on the valve leaflets or valve cusps. The ascending aorta is dilated and the aorta arches to the left before descending along the left side of the vertebral column. There is a small transmural defect (tear) in the wall of ascending aorta. The major arteries arise from the aorta in the usual configuration. The descending aorta gives off the usual branches. The intimal surface of the aorta is smooth. The aorta is elastic and shows moderate atherosclerosis with a defect (tear) in the ascending aorta. The caval veins and portal vein are patent and thin walled. NECK ORGANS: The larynx is lined by smooth mucosa. There is mild epiglottal edema with tracheal microhemmorhages. PULMONARY SYSTEM: The right lung weighs 630 grams and left lung weighs 560 grams. Both lungs appear moderately congested and slightly anthracotic. Dissection of the pulmonary artery reveals no significant pulmonary thromboembolism. A minor small (0.2cm) suspicious thrombus is identified in a small pulmonary vessel. The embolus/thrombus is retrieved, further confirmation of the true nature of the embolus/thrombus pending microscopic examination. The pulmonary veins are unremarkable. The lungs show no infarcts / lesions. The hilar and tracheal bronchial lymph nodes are not enlarged. There is congestion around the pulmonary vasculature as well as in the dependent portion of the lungs. There is no evidence of aspiration. DIGESTIVE SYSTEM: The esophagus courses in the usual fashion to enter the stomach and its mucosal surface is grey-white and intact with longitudinal folds. No lesions are seen grossly. The stomach contains a small amount of thick brown liquid. Its mucosal surface is intact with tall rugal folds. There are few small brown-pink areas of mucosal erythema. The small intestine is of usual caliber and its walls are pliable. The mucosal surfaces are delicate. The appendix is unremarkable. The colon is of generous caliber with intact mucosa. Multiple diverticuli are seen in ascending, descending and transverse colon, with no congestion / hemorrhage (No gross evidence of diverticulitis) No tumor or polyps are found in the gastrointestinal tract. HEPATOBILIARY SYSTEM: The liver is normal sized and weighs 1470 grams with sharp rounded edges. The capsule is smooth and glistening. The parenchyma is solid red-brown and moderately fatty with a tan to yellow hue. The extrahepatic bile ducts and vessels are patent. A discrete gall bladder is not identified. The pancreas is firm and normal in shape. It is located in its usual position within the duodenal sweep and is surrounded by a moderate amount of fat. On sectioning, the parenchyma is tan-brown and lobulated and shows autolysis. The pancreatic duct is patent to the ampulla of Vater. HEMATOPOEITIC SYSTEM/RETICULOENDOTHELIAL SYSTEM: The spleen is large and weighs 120 grams. It has a smooth, intact capsule with blunted edges. The parenchyma is red-brown and congested. ENDOCRINE SYSTEM: The thyroid gland weighs 34.3 grams and has a symmetrical bi-loped shape. The parenchyma is red-brown and firm. Cut surface show soft red glandular tissue with a single nodule (measuring 0.8 x 0.8cm) identified on the left lobe of thyroid. The right and left adrenal glands weigh 5.1 and 5.4 grams respectively. Both adrenals have uniform yellow-orange cortices separated from the medullary gray by a thin red line. URINARY SYSTEM: The kidneys are located in their usual retroperitoneal position. The right kidney weighs 201.0 grams and left kidney weighs 185 grams. External surface shows multiple scars suggestive of nephrosclerosis. There is a single small, fluid filled cyst on the right kidney surface measuring 0.8 x 0.8 cm. Cut sections of the kidneys reveal red-brown parenchyma with clearly demarcated cortico-medullary junctions and cortical thinning. Bilateral ureters are patent to urinary bladder. The ureteral mucosa is smooth. No stones are seen. The bladder is contracted and does not contain urine. The mucosa is intact. The urethra is patent and unremarkable. REPRODUCTIVE SYSTEM: The prostate is enlarged, firm with lobular gray-white parenchyma and has an evident 0.8 cm x 0.8 cm nodule. The testes are located within the scrotal sac bilaterally and have smooth white capsules. The right and left testes weigh 27.9 grams and 30.9 grams respectively. The parenchyma is tan, and the tubules can be strung with ease. MUSCULOSKELETAL: The cartilage is firm. The bone is hard. The vertebrae, ribs, pelvis, and long bones are intact without gross evidence of fracture. The skeletal muscles are red-brown, firm, and appropriate mass for the patient’s age and sex. The bone marrow of the vertebral column is unremarkable. There is no osteoporosis grossly. CENTRAL NERVOUS SYSTEM: Refer to neuropathological report. SUMMARY OF SECTIONS 1A: RIGHT ATRIUM AND VENTRICLE 1B: INFARCT ON THE POSTERIOR WALL OF LEFT VENTRICLE 1C: INFARCT ON THE POSTERIOR WALL OF LEFT VENTRICLE 1D: LEFT VENTRICLE, NORMAL APPEARING 1E: LEFT ATRIUM 1F: PAPILLARY MUSCLE (FROM LEFT VENTRICLE) 1G: INTERVENTRICULAR SEPTUM 1H: MEMBRANOUS CONDUCTION SYSTEM 1I: LEFT ANTERIOR DESCENDING CORONARY ARTERY, FOLLOWING DECALCIFICATION 1J: CORONARY ARTERY GRAFT LEADING TO LAD (INTERNAL MAMMARY), FOLLOWING DECALCIFICATION 1K: LEFT CIRCUMFLEX ARTERY, FOLLOWING DECALCIFICATION 1L: RIGHT UPPER LOBE OF LUNG 1M: RIGHT MIDDLE LOBE OF LUNG 1N: ECCHYMOTIC AREA FROM RIGHT LUNG AND PLEURA 1O: RIGHT LOWER LOBE OF LUNG 1P: LEFT LOWER LOBE OF LUNG 1Q: LEFT UPPER LOBE OF LUNG 1R: THROMBUS FROM A SMALL PULMONARY VESSEL IN LEFT LUNG 1S: LIVER 1T: LIVER (FATTY CHANGE) 1U: SPLEEN 1V: PANCREAS 1W: RIGHT KIDNEY 1X: LEFT KIDNEY WITH PORTION OF THE CORTICAL SCAR 1Y: CYST FROM LEFT KIDNEY 1Z: RIGHT ADRENAL GLAND 1AA: LEFT ADRENAL GLAND 1BB: RIGHT LOBE OF THYROID 1CC: LEFT LOBE OF THYROID (WITH A NODULAR AREA) 1DD: MUSCLE AND NERVE 1EE: BLADDER 1FF: PROSTATE (WITH A NODULAR AREA) 1GG: DESCENDING AORTA, FOLLOWING DECALCIFICATION 1HH: GASTROESOPHAGEAL JUNCTION 1II: STOMACH 1JJ: APPENDIX 1KK: SMALL INTESTINE (ILEUM) 1LL: ASCENDING COLON 1MM: RIGHT TESTES 1NN: LEFT TESTES 1OO: DECALCIFIED BONE 1PP: DECALCIFIED BONE 1QQ: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (MEDIAL) 1RR: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (MEDIAL) 1SS: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (MEDIAL) 1TT: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (LATERAL) 1UU: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (LATERAL) 1VV: RIGHT ATRIUM – ECCHYMOTIC AREA 1WW: RIGHT ATRIUM – ECCHYMOTIC AREA 1XX: RIGHT ATRIUM – ECCHYMOTIC AREA AUTOPSY CHECKLIST ___ Read patient’s chart ___ External Exam ___ Dissection/Gross photos ___ Dictate external exam ___ Rinse organs (next morning) ___ Review with attending ___ Trim case (Bone decal) ___ PAD ___ Dictate Internal exam and Gross description ___ Submit cassettes with decal bone (write cassette range on top of bucket) ___ Check Culture results ___ Slide review/sign out with attending ___ Stains ___ Microscopic description ___ Case Discussion, FAD, final cause of death ___ Submit final report to attending’s worklist MICROSCOPIC DESCRIPTION TEMPLATE HEART: The cardiac myocytes from bilateral ventricles show variation in size and shape, including hypertrophied fibers with enlarged plump nuclei, characteristic of hypertrophy. Interstitial fibrosis is noted bilaterally, and regions of scarring are noted in the interventricular septum. No occlusive atherosclerotic changes are noted in the major coronary arteries with calcifications and recanalization of the occlusion; there is evidence of acute infarction and lymphocytic infiltrates and fibrous adhesions over the epicardium. RESPIRATORY: Sections from the bilateral lungs reveal no emphysematous. Scattered alveolar hemorrhage is noted but with prominent pigment laden macrophages. The sections from lungs show thickened arteries with intimal proliferation, suggestive of pulmonary hypertension. There are no emboli in main pulmonary arteries, but a small pulmonary arteriole shows a small pulmonary thrombo-embolus, showing lines of Zahn. There are no pulmonary infarcts grossly or microscopically. There are scattered foci of interstitial lymphoplasmacytic infiltrates consistent with organizing pneumonia. Diffusely, macrophages laden macrophages are also identified suggestive of congestive cardiomyopathy. HEPATOBILIARY AND PANCREAS: Sections from the liver shows severe autolytic change but no major histopathological abnormality identified. The pancreatic parenchyma displays a normal lobular structure with severe autolysis. GASTROINTESTINAL SYSTEM: The esophagus, and small intestine and the large intestine show normal histology with moderate to severe autolysis. The vessels in the submucosa of the stomach are engorged, consistent with previous episode of bleeding with no histopathological abnormalities. GENITOURINARY SYSTEM: Histologic sections of bilateral kidneys show sclerotic glomeruli and concentric arteriolar thickening suggestive of arteriolar nephrosclerosis. Severe and diffuse autolytic change is noted in the renal tubules. The urinary bladder shows congestion with autolyzed urothelium. Sections from bilateral adnexa are histopathologically unremarkable. RETICULOENDOTHELIAL SYSTEM: The spleen shows normal white and red pulp with moderate congestion. No capsule thickening is identified. MUSCULOSKELETAL: Section of muscle is unremarkable as well as section from peripheral nerve. ENDOCRINE: The thyroid gland shows normal follicular cell and colloid. Adrenal glands show autolytic changes but normal architecture.

ATHEROSCLEROSIS AND ISCHEMIC HEART DISEASE: FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR: CARDIOMEGALY WITH FOUR CHAMBER DILITATION AND HYPERTROPHY (680G) HEMOPERICARDIUM (50CC) WITH TRANSMURAL DEFECT (TEAR) IN THE ASCENDING AORTA S/P THREE VESSEL CORONARY ARTERY BYPASS GRAFT AND PCI SEVERE CORONARY ARTERIOSCLEROSIS MODERATE AORTIC ARTERIOSCLEROSIS RECENT SUB-ENDOCARDIAL POSTERIOR WALL INFART, LEFT VENTRICLE II. RESPIRATORY: PULMONARY CONGESTION AND EDEMA (RIGHT 630G, LEFT 560G) BILATERAL PLEURAL EFFUSIONS (RIGHT 260 CC, LEFT 180 CC) TRACHEAL MICROHEMORRHAGES (LIKELY SECONDARY TO INTUBATION) ATHEROMATOUS PLAQUES OF THE PULMONARY ARTERIES ECCHYMOSIS OF LEFT PLEURA NO EVIDENCE OF PULMONARY EMBOLISM III. GASTROINTESTINAL DIVERTICULOSIS OF COLON (ASCENDING, DESCENDING AND SIGMOID) IV. HEPATOBILIARY FATTY CHANGE OF LIVER IV. ENDOCRINE HISTORY OF DIABETES MELLITUS TYPE II SMALL NODULE ON LEFT LOBE OF THYROID (0.6CM IN GREATEST DIMENSION) V. RENAL BILATERAL RENAL CORTICAL SCARRING (RIGHT 201G, LEFT 185G) SIMPLE CYST IN LEFT KIDNEY (0.9 CM IN GREATEST DIMENSION) VI. GENITOURINARY NODULAR HYPERPLASIA OF THE PROSTATE VII. OTHER VENOUS GRAFT SCARRING, B/L LOWER EXTREMTIY PROVISIONAL / FINAL CAUSE OF DEATH CORONARY, AORTIC AND PULMONARY ATHEROSCLEROSIS, AND ISCHEMIC HEART DISEASE. FINAL NOTE This is a __year-old male with known coronary artery disease, who presented with ongoing progressive chest pain, associated with dizziness, shortness of breath and occasional palpitations. His history of coronary artery disease includes a CABG (x3) in ___. History is significant for Type 2 diabetes, hypertension, hyperlipidemia, obstructive sleep apnea, Graves’ disease, and peripheral neuropathy. In the most recent admission, the patient underwent a redo coronary artery bypass on _/_/_. Postoperative course was complicated secondary to delirium, mild hypotension, and atelectasis (day1), atrial fibrillation (day2). He developed persistent hypotension on day 3 and was acutely desaturated with a pO2 of 67. A CTA was planned on suspicion of a pulmonary embolism. During intubation to protect his airway, the patient suffered a precipitous cardiovascular collapse. During preparing for ECMO, the patient developed irretractable bleeding, with inability to resuscitate the patient, and the patient was pronounced dead at __: __ a.m. Dr. ___ spoke with the patient's wife and permission was given to pursue a complete autopsy. At autopsy, the heart is enlarged and weighs 680 grams with four chamber dilation and hypertrophy, confirmed on microscopic examination. Severe coronary arteriosclerosis with calcification and stenosis is noted upon both gross and microscopic examination, with microscopic evidence of early organizing occluding thrombus in left circumflex coronary artery. Microscopic examination of the posterior wall of left ventricles shows neutrophilic infiltrate, with karyorrhectic debris infiltrating into the necrotic myocytes, with loss of myocyte nuclei and loss of striations, suggestive of a recent myocardial infarction. There is a subendocardial hemorrhage and pericarditis noted in right atrium. The lungs show diffuse congestion with alveolar hemorrhage, diffuse collapse of alveolar spaces and focal mild emphysematous changes. A small pulmonary arteriole shows a small pulmonary thrombo-embolus, showing lines of Zahn. Ascending, transverse, descending and sigmoid colon shows diffuse diverticulosis with no diverticulitis. There is mild steatosis of the liver. Prostate shows nodular hyperplasia. Thyroid shows nodular thyroid with fibrosis and atrophy. Kidney shows mild nephrosclerosis with a simple retention cyst in upper pole of left kidney. The remaining organs were grossly and microscopically unremarkable. The cause of death is severe coronary arteriosclerosis leading to recent as well as remote myocardial infarction. Coronary heart disease (CHD) is a major cause of death and disability in developed countries. Although CHD mortality rates have declined over the past four decades in the United States, CHD remains responsible for about one-third of all deaths in individuals over age 35. It has been estimated that nearly one-half of all middle-aged men and one-third of middle-aged women in the United States will develop some manifestation of CHD. The 2010 heart disease and Stroke Statistics update of the American Heart Association reported that 17.6 million persons in the United States have CHD, including 8.5 million with MI and 10.2 million with angina pectoris. The reported prevalence increases with age for both women and men. Despite the many advances, cardiovascular disease is responsible for more than 2000 deaths every day in the United States. Investigators estimate that 1 of 3 U.S. residents is destined to die of cardiovascular cause. Coronary atherosclerosis is a process that begins early in the patient's life. Epicardial conductance vessels are the most susceptible and intramyocardial arteries, the least. Risk factors for atherosclerosis include elevated plasma levels of total cholesterol and low-density lipoprotein cholesterol (LDL), cigarette smoking, hypertension, diabetes mellitus, advanced age, low plasma levels of high-density lipoprotein cholesterol (HDL), and a family history of premature coronary artery disease. The primary cause of atherosclerotic coronary disease is endothelial injury induced by an inflammatory wall response and lipid deposition. There is evidence that an inflammatory response is involved in all stages of the disease, from early lipid deposition to plaque formation, plaque rupture, and coronary artery thrombosis. Myocardial infarction, the most important form of IHD, in which ischemia causes the death of heart muscle due to reduced blood flow due to obstructive atherosclerotic lesions in the coronary arteries. The prehospital mortality rate for an acute MI (AMI) is approximately 50%. Of those patients who reach the hospital, another 25% die during the hospital stay and another 25% die in the first year afterward. REFERENCES Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics--2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008; 117:e25. Lloyd-Jones DM, Larson MG, Beiser A, Levy D. Lifetime risk of developing coronary heart disease. Lancet 1999; 353:89 Lloyd-Jones D, Adams RJ, Brown TM, et al. Executive summary: heart disease and stroke statistics--2010 update: a report from the American Heart Association. Circulation 2010; 121:948. The clinical anatomy of coronary arteries. Von Lüdinghausen M. Adv Anat Embryol Cell Biol.2003;167:III-VIII, 1-111. Pathologic basis of disease. Robbins and Cotran. 9TH Edition, Chapter 12: The Heart, p. 523-578.

CABG WITH ARRYTHMIA (PAD) FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR: STATUS 3 DAYS POST AORTIC VALVE REPLACEMENT AND CORONARY ARTERY BYPASS GRAFTS; CARDIAC ARREST AND OPEN CHEST RESUSCITATION CARDIOMEGALY WITH FOUR CHAMBER DILATATION AND HYPERTROPHY INCLUDING MARKED LEFT VENTRICULAR HYPERTROPHY (830G) HEMOPERICARDIUM (200CC) WITH MASSIVE INTRATHORACIC HEMORRHAGE. PARTIAL DISRUPTION OF LAD VENOUS BYPASS GRAFT AT ROOT OF ASCENDING AORTA (3M MODERATE CORONARY ARTERIOSCLEROSIS MILD-MODERATE AORTIC ARTERIOSCLEROSIS. BILATERAL BROKEN RIBS S/P RESUSCITATION. II. RESPIRATORY: BILATERAL ATELECTATSIS OF LUNGS (RIGHT 400G, LEFT 300G) B/L PLEURAL EFFUSIONS (RIGHT- SEROSANGUINOUS, 600 CC, LEFT- BLOODY, 1400 CC) MILD ANTHRACOSIS OF LUNGS. SUB-PLEURAL HEMORRHAGE INVOLVING RIGHT MIDDLE LOBE OF LUNG. III. GASTROINTESTINAL: PYLORIC STENOSIS WITH DILATED STOMACH. DIVERTICULOSIS OF COLON. IV. HEPATOBILIARY: HEPATOSPLENOMEGALY WITH FATTY LIVER. (1810G) V. ENDOCRINE: FAT INFILTRATION OF PANCREAS. VI. RENAL: PALE KIDNEYS WITH SWELLING OF CORTEX (SUGGESTIVE OF ATN WITH SHOCK KIDNEY). VII. GENITOURINARY: NODULAR HYPERPLASIA OF THE PROSTATE. DILATED URINARY BLADDER WITH 500 CC OF URINE. PROVISIONAL/FINAL CAUSE OF DEATH CARDIAC ARRHTYHMIA AND ARREST FOLLOWING AORTIC VALVE REPLACEMENT AND CORONARY ARTERY BYPASS GRAFTS.

FINAL NOTE This is a case of a __ y/o Hispanic male with past medical hx of alcoholic cirrhosis, chronic anemia, thrombocytopenia, CAD s/p PTCA and stenting in xxxx, COPD, and endocarditis who presented to the ED complaining of chest pain. Patient stated that he had been sick for the last few months and had been having pain all over. In addition, he reported that he had been having fever. Patient also reported that he has had abdominal pain associated with abdominal distention. The chest pain was located retrosternally and was sharp in nature and associated with shortness of breath especially with laying down. Patient had non-specific ST-T wave changes on EKG. Patient also had Fever and leukocytosis count of 30,000. A CT scan of the abdomen was performed that showed large ascites, cholelithiasis, ground glass opacities in right middle lobe consistent with active airspace disease, and regions of low attenuation within the spleen which could represent splenic infarct. Patient developed sepsis secondary to spontaneous bacterial peritonitis then became bradycardic. Patient went into PEA and was coded for 16 minutes and had ROSC. Patient was transferred to ICU then went into PEA again. The family decided to make the patient DNR during the second code. At autopsy, the skin was jaundiced and there was scleral icterus present. 1 liter of serosanguineous peritoneal fluid was appreciated. There was purulent exudate in the pericardial sac as well. The heart was enlarged, with hypertrophied muscle fibers microscopically. Infective endocarditis was demonstrated with the aortic and tricuspid valves having vegetations that microscopically showed fibrin formation with evidence of bacterial colony formation and inflammation. The spleen showed infarct with inflammation and necrosis and a bacterial colony. The liver was small and nodular, with microscopic disruption of architecture, nodular cirrhosis, steatosis, and obliteration of central veins, which indicate alcoholic cirrhosis. Blood culture, fluid culture, and lung culture showed staphylococcus species, which demonstrates that sepsis was present. Infective endocarditis is defined as an infection the endocardium, which primarily affects the cardiac valves. The incidence is approximately 1 in every 1000 hospital admission and typically, men are affected more commonly than women. There are certain predisposing conditions that can be associated with an increased risk of infective endocarditis. Prosthetic valve, IV drug abuse, congenital abnormality, degenerative valvular disease, and mitral valve prolapse are amongst the more common predisposing conditions. Previous endocarditis is also a predisposing factor as well. About 90% of native valve endocarditis is due to staphylococci, streptococci, or enterococci. Clinically, most patients complain of fever and other non-specific symptoms. Physical examination findings are mostly non-specific, but the presence of Osler’s nodes, and Janeway’s lesions may help physical diagnosis. The leading cause of death in infective endocarditis is heart failure. Embolic events are also relatively common with approximately 35% of cases having evidence of an embolic event. Diagnosis is made clinically because it is difficult to get a culture of a pathologic organism from a valve or other endocardial surface. Antibiotics guided by susceptibilities are the treatment of choice in infective endocarditis, and patients require careful surveillance for the development of complications. Excessive alcohol consumption is associated with a range of hepatic manifestations, including alcoholic fatty liver disease (with or without steatohepatitis), alcoholic hepatitis, and cirrhosis. Patients with an alcohol intake of 30 or more grams per day (one standard drink contains 14 grams of alcohol are at increased risk of cirrhosis, although most patients will not develop cirrhosis despite heavy alcohol intake. Unfortunately, among those who do develop liver disease, symptoms often develop only after severe, life-threatening liver disease has already developed. Alcohol abuse is common world-wide, with an estimated lifetime prevalence of 18 percent among adults in the United States. Alcohol abuse may lead to steatosis, steatohepatitis, cirrhosis, and hepatocellular carcinoma. Once steatohepatitis has developed, the risk of cirrhosis is increased compared with simple steatosis. Patients with alcoholic fatty liver are typically asymptomatic. Patients who have developed cirrhosis may report jaundice, weakness, peripheral edema, abdominal distension, or symptoms of gastrointestinal bleeding, such as hematemesis or melena. Patients with hepatic encephalopathy may note disturbances in their sleep pattern and confusion. Physical examination findings in patients with alcoholic liver disease range from a normal physical examination to evidence of cirrhosis with hepatic decompensation. There are several characteristic laboratory abnormalities in patients with alcoholic liver disease, but none is diagnostic. The classic finding is moderately elevated transaminases, with an aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio >1 (and often >2). The diagnosis is established after excluding other causes of fatty liver or cirrhosis. In patients with cirrhosis, alcohol abstinence decreases the risk of hepatic decompensation and improves survival. Treatment for alcohol use disorders is essential to reduce the likelihood of continued abuse and liver damage. Patients who have decompensated liver disease despite alcohol abstinence should be referred to a liver transplantation center for evaluation. References: Bellentani S, Saccoccio G, Costa G, et al. Drinking habits as cofactors of risk for alcohol induced liver damage. The Dionysos Study Group. Gut 1997; 41:845. Lucey MR, Mathurin P, Morgan TR. Alcoholic hepatitis. N Engl J Med 2009; 360:2758. Chedid A, Mendenhall CL, Gartside P, et al. Prognostic factors in alcoholic liver disease. VA Cooperative Study Group. Am J Gastroenterol 1991; 86:210. O'Shea RS, Dasarathy S, McCullough AJ, et al. Alcoholic liver disease. Hepatology 2010; 51:307. Goldman L, Schafer A. Infective Endocarditis. Goldman’s Cecil Medicine, Twenty-fourth edition. Ch 76, pgs 464-473. Murdoch DR, Corey GR, Hoen B, et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med 2009; 169:463.

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. MODERATE CORONARY ARTERIOSCLEROSIS, LEFT ANTERIOR DESCENDING ARTERY B. LEFT VENTRICULAR HYPERTROPHY C. MEDIASTINAL HEMATOMA, BILATERAL BROKEN RIBS, S/P RESUSCITATION II. RESPIRATORY A. BILATERAL PULMONARY EMBOLI III. OTHER A. MILD NEPHROSCLEROSIS B. COLONIC DIVERTICULA PROVISIONAL CAUSE OF DEATH PULMONARY EMBOLISM AND CORONARY ARTERIOSCLEROSIS, PENDING FURTHER STUDIES FINAL NOTE This is a __ year old male with a past medical history significant for hypertension and hyperlipidemia, who presented to the ED status post unwitnessed syncope and complaining of shortness of breath. En route to the ED the patient went into PEA arrest and CPR was initiated by EMS and administered epinephrine and atropine. The patient had ROSC in approximately 5 minutes. The patient was intubated, and ventilations were maintained. Upon arriving in the ED, the patient had multiple episodes of cardiac arrest and was initiated on an epinephrine drip. Tenecteplase was administered for suspected pulmonary embolus. The patient had ROSC once again, and a CTA was done that showed bilateral pulmonary emboli. Prior to transferring the patient to the ICU, the patient's blood pressure dropped and went into another cardiac arrest. During this time, the wife requested that CPR be stopped, and the patient was pronounced dead on 12/15/2014 at 13:05. Consent for a limited autopsy was requested and attained to determine the cause of death. At the time of autopsy, the external exam was grossly normal except that it was noted that the eyes had been harvested for donation. Internally, broken ribs and hemorrhage from resuscitation were noted. The heart was slightly enlarged at 410 grams, with hypertrophied muscle fibers on microscopy. There was coronary arteriosclerosis present within the LAD, LCX, and to a lesser extent in the RCA. Examination of the lungs demonstrated small, bilateral pulmonary emboli within the arteries with the largest measuring 0.5cm in greatest dimension in the right lung. The remaining lung parenchyma was unremarkable. An incidental hemangioma measuring 1.0cm was discovered on examination of the liver. The kidneys had mild nephrosclerosis as well. No underlying malignancy (a possible cause of hypercoagulable state) was identified after examining representative samples of all organ systems. Note is made of the radiologic studies that were performed that showed that there was a deep vein thrombosis in the patient's leg. Much of the pathology in this case rested within the lungs in the form of pulmonary emboli. Acute pulmonary embolism (PE) is a common disease with mortality rate as high as 30% if left untreated (1). Prompt diagnosis and treatment can reduce mortality, but the presenting symptoms are often nonspecific and vague. A massive pulmonary embolus is defined by a systolic blood pressure <90mmHg or a drop in systolic blood pressure by >40mmHg for greater than 15 minutes (1). Index of suspicion should be high any time there is hypotension with elevated central venous pressure not explained by other entities. Massive pulmonary embolism is a high-mortality event which can result in right ventricular failure and sudden death (1). Incidence of pulmonary embolism is hard to quantitate because more than half of all pulmonary emboli probably go undiagnosed; one study examined 42 million deaths over a 20-year period and found that approximately 600,000 had been diagnosed with PE and of these, 200,000 had PE as cause of death (approximately 0.47%) (1). The incidence is expected to rise with the utilization of computed tomographic pulmonary angiography (CT-PA). There are multiple factors involved in determining the prognosis of PE. Right ventricular dysfunction, right ventricular thrombus, deep vein thrombosis, elevated brain natriuretic peptide, elevated serum troponin, hyponatremia, and elevated lactate levels are all associated with increased mortality (1). The Pulmonary Embolism Severity Index (PESI) and the Simplified Pulmonary Embolism Severity Index (sPESI) are prognostic models utilized to stratify patients for thrombolytic therapy based on their risk factors and symptoms. Most pulmonary thromboemboli originate in the deep venous system of the lower extremities, especially the iliofemoral veins; right heart, pelvic, renal, and upper extremity veins are less common sites of origin (1). Most pulmonary emboli are multiple with predilection for lower lobes. Hypotension manifests when cardiac output is reduced by increased pulmonary vascular resistance; eventually the right ventricle is unable to overcome the increased pressure and cannot maintain pulmonary perfusion (1). There are many well-recognized risk factors for pulmonary embolism. Immobilization, surgery (within 3 months), stroke, paralysis, central venous instrumentation (within 3 months), malignancy, chronic heart disease, autoimmune disease, and a history of venous thromboembolism all increased risk of pulmonary embolism (1). In addition, women who are obese (BMI ≥29), heavy cigarette smokers (>25 cigarettes/day), and hypertensive are at an even greater risk (1). A 1992 chronobiological study out of Italy examined 507 consecutive sudden deaths that occurred outside the hospital; at autopsy 48 of them were found to have fatal pulmonary emboli and of these patients, circadian and circannual rhythmicity showed statistically significant predilection for morning and winter (2). The Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) looked at 824 patients without underlying cardiopulmonary disease and determined that the most common presenting symptoms of PE are dyspnea, pleuritic pain, cough, >2 pillow orthopnea, calf or thigh pain, calf or thigh swelling, and wheezing; the most common signs are tachypnea, tachycardia, rales, decreased breath sounds, accentuated pulmonic component of the second heart sound, and jugular venous distension (3). However, pulmonary embolism is frequently asymptomatic as demonstrated by a review of 5233 patients with deep vein thrombosis, 32% of which had asymptomatic PE (1). When symptoms are present, shock or hypotension is the principal prognostic marker and indicates a high-risk of death (30-50%) (1). The patient in this case appears to have developed a DVT within the lower extremity that then manifested in the form of pulmonary embolism. Internal and external examination revealed multiple bilateral emboli consistent with the antemortem CT findings. Microscopic examination demonstrated multiple small bilateral emboli but note should be made that the patient received Tenecteplase which could have broken up a larger embolus that would explain the acute symptoms in this case. The unexpected sudden death of the patient in this case is explained by pulmonary thromboembolism which was exacerbated by the underlying coronary artery disease within the heart. References: Thompson, T., and Hales, C., "Overview of Acute Pulmonary Embolism". UpToDate. Jul 2014. Gallerani, M., et al "Sudden Death from Pulmonary Thromboembolism: Chronobiological Aspects". Eur Heart J. 1992: 13(5):661-665. Stein, P., et al "Multidetector Computer Tomography for Acute Pulmonary Embolism". NEJM. 2006:354(22):2317-2327.

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. CARDIOMEGALY (410G) CONSISTENT WITH HYPERTENSIVE CARDIOMYOPATHY B. MYOCARDIAL FIBROSIS AND OLD SUBENDOCARDIAL INFARCT II. RESPIRATORY A. ORGANIZED BRONCHOPULMONARY PNEUMONIA WITH ABSCESS FORMATION B. DIFFUSE ALVEOLAR DAMAGE C. BILATERAL PULMONARY ADHESIONS III. GENITOURINARY A. LEFT RENAL AGENESIS B. RIGHT KIDNEY HYPERTROPHY WITH EXTENSIVE NEPHROSCLEROSIS C. DOUBLE RIGHT RENAL ARTERIES IV. OTHER A. CHRONIC PANCREATITIS WITH FAT NECROSIS B. UTERINE FIBROID C. LEFT PARATUBAL CYST D. MALFORMED LEFT OVARY FINAL CAUSE OF DEATH BILATERAL NECROTIZING PNEUMONIA AND SEPSIS FINAL NOTE This is a ___ year old female with a past medical history of osteoarthritis and C3-C4 fusion, who was found down obtunded in her apartment after her landlord noticed she was absent for 5 days. She was transferred to ___ hospital where she was diagnosed with urosepsis and chest X-ray showing bilateral nodular opacities and metabolic acidosis. She quickly deteriorated and required intubation. A CT of the head was done that showed normal pressure hydrocephalus. The patient became hypotensive and pressors and hydration were started. She was transferred to ___ hospital. The patient was treated for UTI/bacteremia. The patient soon developed ARDS and was unable to ventilate or oxygenate. As her respiratory failure worsened, she also developed pneumothorax for which chest tubes were placed. The patient was placed on ECMO for oxygenation. The patient also developed stress hyperglycemia and was treated with insulin drip. The patient remained obtunded despite being off all sedation. Another head CT noted that the patient had a small petechial subarachnoid hemorrhage. Anticoagulation was stopped at this point and a chest CT was performed that showed diffuse bilateral ground glass opacities and diffuse lesions. A follow up CT during her course showed new cavitary lesions and increasing size in previous lesions. The patient was also in acute renal failure and required CVVH. Thrombocytopenia was also a complicating factor during the hospital course. The patient continued to be hypoxic and hypotensive despite medical intervention. It was felt that further care was futile, and this was discussed with the family. CVVH was stopped at -: -- pm on --/--/-- and ECMO was stopped at -: --pm on --/--/--. The patient was pronounced dead at --: --pm on --/--/-- and consent for a full autopsy with no restrictions was requested and attained to determine the cause of death. At autopsy, the external examination was unremarkable. On internal examination, it was noted that the left kidney was absent. The heart appeared mildly enlarged. The lungs had abundant bilateral abscesses. There were no pulmonary emboli noted. No vegetations were noted on the heart valves. Cultures of the blood were sterile, but lung tissue culture grew Enterococcus species, Yeast, and Bacteroides fragilis. Microscopic examination demonstrated hypertrophic changes within the heart. There was also evidence of old subendocardial infarct. There were hypertensive changes within the coronary arteries. Sections from the lungs showed evidence of organized bronchopulmonary pneumonia forming multiple abscesses with a mixed inflammatory infiltrate. Gram stain was positive for sparse gram-positive diplococci in short chains. GMS was negative. The rest of the lung parenchyma was severely congested with diffuse alveolar damage. The pancreas section showed autolysis and an inflammatory infiltrate consistent with chronic pancreatitis with areas of fat necrosis. Kidney sections demonstrated nephrosclerotic changes including glomerulosclerosis and interstitial fibrosis. There was no evidence of acute infection. Urinary bladder sections showed a mild lymphocytic infiltrate within the urothelium. Sections from the muscle show atrophic muscle fibers and regenerative changes with an inflammatory infiltrate. Lung abscess is defined as necrosis of the pulmonary parenchyma caused by microbial infection. Some authorities use the term "necrotizing pneumonia" or "lung gangrene" to distinguish pulmonary necrosis with multiple small abscesses from a larger cavitary lesion, but this represents a continuum of the same process. Most lung abscesses arise as a complication of aspiration pneumonia and are caused by species of anaerobes that are normally present in the gingival crevices. The typical patient has a predisposition to aspiration due to compromised consciousness (e.g., alcoholism, drug abuse, general anesthesia) or dysphagia. These patients also frequently have periodontal disease, especially gingivitis. The first step in the development of a lung abscess is for the inoculum from the gingival crevice to reach the lower airways, which usually occurs while the patient is in the recumbent position. Infection is initiated either because the bacteria are not cleared due to suppressed consciousness or because the inoculum size is large due to dysphagia. Pneumonitis arises first but based upon the usual mixture of organisms, progresses to tissue necrosis after 7 to 14 days. This necrosis results in lung abscess and/or an empyema. Lung abscess is caused most frequently by bacteria, usually anaerobes. The bacteria in lung abscess reflect the predominantly anaerobic flora of the gingival crevice. The most common organisms are Pepto streptococcus, Prevotella, Bacteroides, and Fusobacterium spp. Most patients with lung abscesses, and nearly all with lung abscesses due to anaerobic bacteria, present with indolent symptoms that evolve over a period of weeks or months. The characteristic features suggest pulmonary infection, including fever, cough, and sputum production. Evidence of chronic systemic disease is usually present, with night sweats, weight loss, and anemia. Patients may seek medical attention for these systemic symptoms, hemoptysis, or pleurisy. Nearly all patients have fever, but virtually none have shaking chills or true rigors. Chest radiographs usually show infiltrates with a cavity, frequently in a segment of the lung that is dependent in the recumbent position. The most important component of the evaluation of a lung abscess is to define the probable etiologic agent to select appropriate antibiotic therapy and to detect associated conditions, such as malignancy. A chest radiograph will generally demonstrate the pulmonary lesion to the extent necessary for diagnosis and management. However, better anatomic definition can be achieved with computed tomographic (CT) scans. References: 1. Bartlett JG. Lung abscess and necrotizing pneumonia. In: Infectious Diseases, Gorbach SL, Bartlett JG, Blacklow NR (Eds), W.B. Saunders, Philadelphia 1992. 2.Chung G, Goetz MB. Anaerobic Infections of the Lung. Curr Infect Dis Rep 2000; 2:238.

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. CARDIOMEGALY (400G) B. PATENT FORAMEN OVALE C. LEFT VENTRICULAR HYPERTROPHY (1.9CM) II. RESPIRATORY A. ACUTE BRONCHOPULMONARY PNEUMONIA WITH YEAST B. EMPHYSEMATOUS CHANGES WITH ANTHRACOSIS C. HYALINIZED ALVELOAR MEMBRANES III. HEPATOBILIARY A. CIRRHOSIS WITH EXTENSIVE STEATOSIS AND MILD LOBULAR INFLAMMATION B. BILE STASIS AND BILE DUCT PROLIFERATION C. JAUNDICE AND SCLERAL ICTERUS D. ASCITES (1800CC) FINAL CAUSE OF DEATH LIVER FAILURE DUE TO CIRRHOSIS WITH MARKED FIBROSIS AND STEATOSIS FINAL NOTE This is a __year old {male/female} with a reported past medical history significant for Hepatitis C, cirrhosis, and prior IV drug abuse who presented to ___ Hospital with abdominal pain and altered mental status. Per the fiancé and mother, the patient had not been feeling well for the past 2 weeks. She reported general malaise, jaundice, anorexia, and decreased urination. She was brought to the ED by her fiancé when he was unable to arouse her. She was intubated and transferred to ___ Hospital due to her renal and liver failure. She received 2 units of blood and an NG tube suctioned 250ml of bright red blood. Her SBP was in the 60’s so she had a femoral line placed and started on Levophed for shock. She received 4 liters of normal saline. The patient was hypoglycemic and hypothermic, and the patient was also started on CVVH. The patient died at --: -- on --/--/---- and consent for an autopsy was requested and attained to determine the cause of death. At autopsy, the skin was noted to be jaundiced and there was prominent scleral icterus. The heart was found to have a slightly patent foramen ovale and was enlarged, weighing 400 grams. Microscopically, there was evidence of hypertrophy. The lungs were grossly unremarkable, but histologically appeared to have acute bronchopulmonary pneumonia with yeast that were highlighted by GMS and PAS stains. There was also evidence of hyaline membranes that are indicative of diffuse alveolar damage associated with a respirator. There was also histologic evidence of emphysema and anthracosis. The liver was grossly cirrhotic, green, and nodular. There was associated ascites (1800cc). Microscopically, the liver had marked fibrosis, steatosis, and bile stasis. There was some lobular inflammation noted as well. There are numerous causes of liver disease that can result in cirrhosis, either by causing chronic hepatic inflammation or cholestasis. The two most common causes of cirrhosis in the United States are alcoholic liver disease and hepatitis C. The clinical manifestations of cirrhosis may include nonspecific symptoms (e.g., anorexia, weight loss, weakness, fatigue) or signs and symptoms of hepatic decompensation (jaundice, pruritus, signs of upper gastrointestinal bleeding, abdominal distension from ascites, confusion due to hepatic encephalopathy). Physical examination findings may include jaundice, spider angiomas, gynecomastia, ascites, splenomegaly, palmar erythema, digital clubbing, and asterixis. Laboratory abnormalities may include elevated serum bilirubin, abnormal aminotransferases, elevated alkaline phosphatase/gamma-glutamyl transpeptidase, a prolonged prothrombin time/elevated international normalized ratio (INR), hyponatremia, and thrombocytopenia. In patients suspected of having cirrhosis, abdominal imaging is typically obtained, though radiographic imaging alone is not adequately sensitive or specific to diagnose cirrhosis. The findings must be viewed in light of other signs of cirrhosis such as physical examination or laboratory test findings. A liver biopsy is required to definitively confirm the diagnosis of cirrhosis. However, it is generally not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and the results would not alter the patient's management. Determining the etiology of cirrhosis is important because it may influence treatment decisions, permit counseling of family members, and help predict the patient's prognosis. The initial evaluation includes obtaining a history, performing a physical examination, and obtaining routine blood tests (i.e., liver biochemical and function tests and a complete blood count). The findings from the initial evaluation are then used to guide additional testing. In this case, the cause of death was liver failure due to cirrhosis. The differential diagnosis for cirrhosis is extensive and the patient in this case did not have previous documentation at Hartford Hospital that was positive for hepatitis C. Although the social history states that there was a history of hepatitis C, the gross and histologic findings suggest that the cirrhosis may have had an alcohol etiology. Unfortunately for this patient, knowing the etiology of the cirrhosis may not have improved the prognosis because of the extent of the cirrhosis. REFERENCES 1. Goldberg E, Chopra S. Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis. In: UpToDate, Runyon, B (Ed). Retrieved from http://www.uptodate.com/home 2. Friedman, S. Clinical manifestations and diagnosis of alcoholic fatty liver disease and alcoholic cirrhosis. In: UpToDate, Runyon, B (Ed). Retrieved from http://www.uptodate.com/home 3. O'Shea RS, Dasarathy S, McCullough AJ, et al. Alcoholic liver disease. Hepatology 2010; 51:307. 4. Heidelbaugh JJ, Bruderly M. Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation. Am Fam Physician 2006; 74:756.

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. CARDIOMEGALY (490G) WITH LEFT VENTRICULAR HYPERTROPHY B. ACUTE AND OLD MYOCARDIAL INFARCTION C. SEVERE CORONARY ARTERIOSCLEROSIS; (LAD:90%, LCX:50%, RCA:50%) D. S/P ABDOMINAL AORTIC GRAFT BELOW RENAL ARTERIES E. ANEURYSMAL AORTIC DILATATION WITH INTRAMURAL THROMBUS PROXIMAL TO GRAFT F. PARTIAL THROMBOTIC OCCLUSION OF RENAL ARTERY OSTIA G. PARTIAL THROMBOTIC OCCLUSION OF CELIAC AND MESENTERIC ARTERY OSTIA II. RESPIRATORY A. BILATERAL HYALINIZED AND CALCIFIED DIAPHRAGMATIC PLEURAL PLAQUES B. LEFT LUNG ADHESIONS C. FOCUS OF METAPLASTIC OSSIFICATION III. HEPATOBILIARY A. HEPATIC INFARCTS ASSOCIATED SEVERE HEPATIC CONGESTION B. HEPATIC VEIN THROMBUS C. PANCREATIC ISCHEMIA IV. GASTROINTESTINAL A. MESENTERIC THROMBUS WITH SEGMENT OF GANGRENOUS LARGE AND SMALL INTESTINE B. GASTRIC MUCOSAL ERYTHEMA WITH SUPERFICIAL GASTRITIS C. LOWER GI HEMORRHAGE V. GENITOURINARY A. SEVERE BILATERAL RENAL ATROPHY AND NEPHROSCLEROSIS (RIGHT 62G, LEFT 85G) B. TESTICULAR HYDROCELE VI. HEMATOPOETIC A. LOW GRADE LYMPHOPROLIFERATIVE DISORDER OF BONE MARROW VII. OTHER A. BILATERAL LOWER EXTREMITY PITTING EDEMA B. SEVERE SPINAL OSTEOARTHRITIS C. MILD ADRENAL CORTICAL HYPERPLASIA FINAL CAUSE OF DEATH INTESTINAL AND HEPATIC INFARCT SECONDARY TO SEVERE ABDOMNIAL AORTIC ATHEROSCLEROSIS AND DILATATION FINAL NOTE This is a __y/o male with a past medical history significant for CAD, HTN, and AAA repair in 19__, who presented to the ED on __/__/___ with dyspnea on exertion, confusion, and 40-pound weight loss over 8 months. In the ED he was found to have acute kidney injury, hyperkalemia, severe normocytic anemia, anion gap lactic acidosis, and NSTEMI. He was transferred to ICU for developing hypoxia, altered mental status, and hypotension. He was noted to be afebrile but have retro-cardiac opacification on CXR. He was started on vasopressors, antibiotics. He was also noted to have possible DIC with decreased platelets, and increased PTT. He developed worsening respiratory status and hypotension requiring max ventilator settings and maximal amount of vasopressors. The patient was DNR status and died at __: __am on __/__/___ and consent for a full autopsy with no restrictions was requested and attained to determine the cause of death. At autopsy, external examination demonstrated severe pitting edema and testicular hydrocele. Examination of the heart showed cardiomegaly and severe coronary arteriosclerosis and associated acute and old myocardial infarction. In the aorta, there was aneurysmal dilatation with atherosclerosis and intramural thrombus noted proximal to the aortic graft. The thrombus was noted to be partially occluding the renal artery ostia and almost completely occluding the celiac and mesenteric artery ostia. In the lungs, there were bilateral hyalinized and calcified diaphragmatic plaques. There were also lung adhesions noted. In the liver, there were multiple areas of infarct associated with hepatic vein thrombus. There was infarct noted within the pancreas as well. There was a mesenteric thrombus noted and the intestines were found to be gangrenous. The kidneys were bilaterally atrophic and had severe nephrosclerosis. Incidentally, there was a low-grade B-cell lymphoma found within the vertebral bone marrow. In this case, the cause of death was multi-organ infarct secondary to severe abdominal aortic atherosclerosis and dilatation. Abdominal aortic aneurysm (AAA) is the most common true arterial aneurysm. A true aneurysm is defined as a segmental, full-thickness dilation of a blood vessel that is 50 percent greater than the normal aortic diameter. False aneurysms of the abdominal aorta can also occur but are much less common. In most adults, an aortic diameter >3.0 cm is generally considered aneurysmal. Normal aortic diameter varies with age, gender, and body habitus, but the average diameter of the adult human infrarenal aorta is about 2.0 cm and typically less than 3.0 cm. Thus, for most patients, an infrarenal aorta with a maximum diameter ≥3.0 cm is aneurysmal. Well-defined clinical risk factors are associated with the development of AAA. These include advancing age, male gender, smoking, Caucasian race, a family history of AAA, the presence of other large aneurysms, and atherosclerosis. Smoking is a major risk factor for aneurysm formation. A history of cigarette smoking is one of the strongest independent risk factors for AAA. Patients with AAA have a significantly higher prevalence of risk factors for atherosclerosis compared with age and gender-matched controls. The indications for repair of abdominal aortic aneurysm (AAA) include symptomatic aneurysm of any size (e.g., abdominal, back or flank pain, evidence of embolization, frank rupture), asymptomatic aneurysm ≥5.5 cm, rapidly expanding AAA, AAA associated with other arterial disease, infected AAA, and complications following endovascular repair necessitating early or late conversion to an open AAA repair. All aortic aneurysms have some degree of mural thrombus and cholesterol plaque, which have the potential to dislodge and embolize during aortic dissection and clamping. However, thromboembolism is uncommon with elective AAA repair. Colonic ischemia is uncommon following elective AAA repair. Pelvic arterial inflow should be preserved to at least one vessel (inferior mesenteric artery, right internal iliac artery, left internal iliac artery). For patients who survive open AAA repair, the main cause of death in the long term is cardiovascular disease. Perioperative complications related to the aortic procedure include lower extremity ischemia, bowel ischemia, pelvic ischemia, renal dysfunction, and late complications include incisional hernia, anastomotic aneurysm, and graft infection/aortoenteric fistula. In this case, the patient died of multi-organ infarct secondary to severe abdominal atherosclerosis and dilatation. The history of AAA in this case was a major factor in the pathogenesis of the atherosclerosis and intramural thrombus that ultimately occluded the ostia to major organs. Incidentally, a low-grade B-cell lymphoma was discovered in the vertebral bone marrow at autopsy. It is unclear if this played any role in the progression of disease in this patient, but it is unlikely since the lymphoproliferative disorder was not apparent in laboratory studies. References: 1. Mohler, E. Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm. Mills, J (Ed.). UpToDate.com/home. Current through January 2015. 2. Collins, K. Overview of abdominal aortic aneurysm. Eidt, J (Ed.). UptoDate.com/home. Current through January 2015. 3. Eidt, J. Open surgical repair of abdominal aortic aneurysm. Mills, J (Ed.). UptoDate.com/home. Current through January 2015. 4. Chaikof EL, Brewster DC, Dalman RL, et al. SVS practice guidelines for the care of patients with an abdominal aortic aneurysm: executive summary. J Vasc Surg 2009; 50:880.

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. BIATRIAL DILATATION AND LEFT VENTRICULAR HYPERTROPHY (2.1CM) B. CORONARY ARTERIOSCLEROSIS (LAD 40%, LCX 30%, RCA 30%) II. HEMATOPOIETIC AND LYMPHOVASCULAR A. CLASSICAL HODGKIN’S LYMPHOMA INVOLVING LYMPH NODES AND SPLEEN III. RESPIRATORY A. PULMONARY HYPERTENSION B. EMPHYSEMATOUS CHANGES WITH ANTHRACOSIS C. DIFFUSE INTERSTITIAL FIBROSIS IV. HEPATOBILIARY A. DISTENDED GALLBLADDER (30CC OF BILE) WITH CHOLELITHIASIS B. MILD HEPATIC STEATOSIS V. GENITOURINARY A. BILATERAL NEPHROSCLEROSIS (R: 105G, L: 95G) B. NODULAR GLOMERULOSCLEROSIS SUSPICIOUS FOR DIABETIC NEPHROPATHY VI. GASTROINTESTINAL A. DIVERTICULOSIS COLI WITH BOWEL WALL THICKENING B. DIVERTICULUM, SMALL INTESTINE VII. ENDOCRINE A. THYROID ATROPHY B. ADRENAL CORTICAL ATROPHY VIII. OTHER A. ANTEMORTEM BLOOD CULTURES POSITIVE X2 FOR MRSA FINAL CAUSE OF DEATH SEPSIS DUE TO IMMUNCOMPROMISED STATE (HODGKIN’S LYMPHOMA) FINAL NOTE This is a __ year old male/female with a past medical history significant for CVA, dementia, atrial fibrillation, HTN, TIA, and depression who presents with 3 weeks of generalized and worsening weakness, lethargy, weight loss, decreased oral intake. The patient also had nausea and diarrhea for 2-3 days prior to presentation at ___ Hospital. She was found to be in sepsis and a CT scan showed a distended gallbladder with sludge, retroperitoneal lymphadenopathy, and mild diverticulitis. The patient was transferred to ___Hospital for further care and her confusion worsened after admission. She became hypotensive and apneic and died on __/__/___ at __: __ AM. Autopsy consent was requested and obtained to determine the cause of death. At autopsy, it was noted that the patient appeared somewhat cachectic and older than the stated age of 76 years of age. On internal examination, there was severe gross lymphadenopathy in the mediastinum, supraclavicular area, para-tracheal, and para-aortic areas. There was some dilatation of the cardiac atria noted bilaterally. Some coronary arteriosclerosis was identified as well. Within the lungs, some emphysematous changes were noted. The gallbladder was distended with 30cc of bile and multiple choleliths. The kidneys appeared nephrosclerotic. There was also atrophy of the thyroid and the adrenal cortex noted. On microscopic examination, the most striking finding was within the spleen and lymph nodes. Representative spleen and lymph node sections show effacement of the normal architecture. There is a mixed inflammatory infiltrate admixed with classic Reed-Sternberg cells that appear large with basophilic cytoplasm and have at least two nuclear lobes. The RS cells are positive for CD30 and PAX-5 while being negative for CD15, CD20, and EBER. The kidneys microscopically had nephrosclerosis but were also found to have hyalinized nodules within many of the glomeruli which raised the suspicion for diabetic nephropathy. The cause of death in this was sepsis due to an immuno-compromised state of Hodgkin’s Lymphoma. Hodgkin lymphoma (HL), formerly called Hodgkin's disease, arises from germinal center or post-germinal center B cells. HL has a unique cellular composition, containing a minority of neoplastic cells (Reed-Sternberg cells and their variants) in an inflammatory background. It is separated from the other B cell lymphomas based on its unique clinicopathologic features. The tumor cells in this group are also derived from germinal center B cells, but typically fail to express many of the genes and gene products that define normal germinal center B cells. Based on differences in the appearance of the tumor cells and the composition of the reactive background, classical HL is further divided into the following subtypes: 1) Nodular sclerosis classical HL (NSHL), 2) Mixed cellularity classical HL (MCHL), 3) Lymphocyte rich classical HL (LRHL), 4) Lymphocyte depleted classical HL (LDHL). Hodgkin lymphoma (HL) accounts for approximately 10 percent of all lymphomas and approximately 0.6 percent of all cancers diagnosed in the developed world annually. HL has a bimodal age distribution curve. The pattern of age-specific incidence differs by geographic location and appears to parallel the level of industrial development. The predominant histologic subtype also differs by geographic location and economic advancement. In developed countries such as the US, nodular sclerosis HL (NSHL) is the predominant histologic subtype and accounts for most of the peak in young adults. In economically disadvantaged areas, mixed cellularity HL (MCHL) is more frequent in children and older adults. Early industrialized or transitional economies tend to have an equal frequency of MCHL and NSHL subtypes. Classical HL is a heterogeneous group of tumors characterized by the presence of a minority of neoplastic cells (Reed-Sternberg cells and their variants) in an inflammatory background. Diagnostic RS cells are large cells with slightly basophilic cytoplasm that have bilobed, double, or multiple nuclei and prominent, eosinophilic, inclusion-like nucleoli in at least two nuclei or nuclear lobes. Detection of EBV can be helpful in the differential diagnoses of classical HL and other lymphomas, which are uniformly EBV negative. The diagnosis of HL is made by the evaluation of involved tissue, usually a lymph node biopsy. Excisional biopsies are preferred, and large core needle biopsies may be adequate in select cases, but fine needle aspiration alone does not provide enough tissue or information on the structural composition of the lymph node to provide an accurate diagnosis. Evaluation of the biopsy material should include both routine light microscopy and analysis of the immunophenotype with immunohistochemistry. The differential diagnosis of classic HL includes nodular lymphocyte predominant HL and varieties of non-Hodgkin lymphoma that may have similar clinical presentations or morphology. In this case, there was no previous history of lymphoma noted so the diagnosis of classical Hodgkin’s Lymphoma is being made at autopsy. The patient ultimately died of sepsis due to MRSA, (confirmed with antemortem blood cultures) but it was the Hodgkin’s Lymphoma that caused the patient to be in an immunocompromised state. REFERENCES 1. Aster, J. Epidemiology, pathologic features, and diagnosis of classical Hodgkin lymphoma. Freedman, A (Ed.). Uptodate.com/home. January 2015. 2. Mauch, P. Clinical presentation and patterns of disease distribution in classical Hodgkin lymphoma in adults. Freedman, A. (Ed.). Uptodate.com/home. January 2015. 3. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2015. CA Cancer J Clin 2015; 65:5. 4. Mauch PM, Kalish LA, Kadin M, et al. Patterns of presentation of Hodgkin disease. Implications for etiology and pathogenesis. Cancer 1993; 71:2062. 5. Kaplan HS. Hodgkin's Disease, 2nd ed, Harvard University Press, Cambridge, MA 1980.

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. CARDIOMEGALY (510G) B. SEVERE CORONARY ARTERIOSCLEROSIS; LAD 70%, LCX 60%, RCA 90% C. LEFT VENTRICULAR HYPERTROPHY (1.8CM) D. AORTIC ATHEROSCLEROSIS II. RESPIRATORY A. BILATERAL LUNG CONGESTION (R: 1080G, L: 850G) B. PULMONARY HYPERTENSION III. HEPATOBILIARY A. HEPATIC STEATOSIS IV. GENITOURINARY A. BILATERAL NEPHROSCLEROSIS FINAL CAUSE OF DEATH SEVERE CORONARY ARTERIOSCLEROSIS FINAL NOTE This is a __year old female with a past medical history significant for CAD, stable angina, HTN, hyperlipidemia, and diabetes who presented to the ED after being found down at home for an unknown time. First responders arrived on scene and found the patient to be in a shockable rhythm. The patient had return of circulation and was intubated and brought to ___ Hospital. She was then subsequently transferred to ___ Hospital for hypothermia protocol. Upon arrival to ___ Hospital, the patient was found to be completely unresponsive to all stimuli. Her pH was 6.89 on blood gas. She was also found to be hyperglycemic with glucose levels over 500. The patient continued to deteriorate and was maxed on three pressors. The patient was placed on CVVH but continued to have multi-organ failure. The patient died on __/__/____ at __: __ AM and consent for an autopsy was obtained to determine the cause of death. At autopsy, the heart is enlarged at 510 grams with left ventricular hypertrophy, confirmed on microscopic examination. Severe coronary arteriosclerosis with calcification and stenosis is noted upon both gross and microscopic examination. Microscopic examination of the left ventricular wall and anterior papillary muscles shows fibrotic scarring which indicates old myocardial infarct. There is also acute ischemic change noted as well. The lungs appear grossly congested with alveolar hemorrhage and microscopic examination shows thickened small blood vessels, which are suggestive of pulmonary hypertension. There was mild steatosis of the liver. The remaining organs were grossly and microscopically unremarkable. The immediate cause of death is severe coronary arteriosclerosis. Myocardial infarct due to the severe coronary artery disease contributed to the cause of death. Coronary heart disease (CHD) is a major cause of death and disability in developed countries. Although CHD mortality rates have declined over the past four decades in the United States, CHD remains responsible for about one-third of all deaths in individuals over age 35. It has been estimated that nearly one-half of all middle-aged men and one-third of middle-aged women in the United States will develop some manifestation of CHD. The 2010 heart disease and Stroke Statistics update of the American Heart Association reported that 17.6 million persons in the United States have CHD, including 8.5 million with MI and 10.2 million with angina pectoris. The reported prevalence increases with age for both women and men. The exact mechanism of collapse in an individual patient is often impossible to establish since, for most patients who die suddenly, cardiac activity is not being monitored at the time of their collapse. As a result, the mechanism can only be inferred, based upon information obtained after the process has been initiated. Sudden Cardiac Death (SCD) refers to sudden cessation of cardiac activity with hemodynamic collapse, typically due to sustained ventricular tachycardia/ventricular fibrillation. These events mostly occur in patients with structural heart disease (that may not have been previously diagnosed), particularly coronary heart disease. There is a clear relationship between SCD and CHD. Clinical and autopsy studies and data from death certificates have found that 62 to 85 percent of patients who suffer out-of-hospital SCD have evidence of prior CHD, 10 percent have other structural cardiac abnormalities, and 5 percent have no structural cardiac abnormality. Although the risk of SCD is highest in patients with a history of SCD, a prior MI, or heart failure, approximately 80 percent of SCD events occur in asymptomatic patients who do not have a prior history of CHD or MI. REFERENCES 1. Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics--2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008; 117: e25. 2. Lloyd-Jones D, Adams RJ, Brown TM, et al. Executive summary: heart disease and stroke statistics--2010 update: a report from the American Heart Association. Circulation 2010; 121:948. 3. Lloyd-Jones DM, Larson MG, Beiser A, Levy D. Lifetime risk of developing coronary heart disease. Lancet 1999; 353:89. 4. American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology), Buxton AE, Calkins H, et al. ACC/AHA/HRS 2006 key data elements and definitions for electrophysiological studies and procedures: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology). Circulation 2006; 114:2534. 5. Demirovic J, Myerburg RJ. Epidemiology of sudden coronary death: an overview. Prog Cardiovasc Dis 1994; 37:39.

CIRRHOSIS AND CORONARY ARTERIOSCLEROSIS WITH ACUTE AND OLD MYOCARDIAL INFARCT FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. MYOCARDIAL HYPERTROPHY B. ACUTE AND OLD MYOCARDIAL INFARCT C. CORONARY ARTERIOSCLEROSIS (LAD 50%, LCX 40%, RCA 65%) II. RESPIRATORY A. PULMONARY HYPERTENSION B. DIFFUSE ALVEOLAR DAMAGE WITH HYALINE MEMBRANES C. EMPHYSEMATOUS AND ANTHRACOTIC CHANGES III. HEPATOBILIARY A. NODULAR CIRRHOSIS WITH REGENERATIVE NODULE B. STEATOSIS AND MILD LOBULAR INFLAMMATION C. MILD HEPATIC AND PANCREATIC HEMOSIDERIN DEPOSITION D. JAUNDICE AND SCLERAL ICTERUS IV. GENITOURINARY A. BILATERAL NEPHROSCLEROSIS B. CHRONIC UROCYSTITIS IV. OTHER A. SPLENOMEGALY (390G) B. ESOPHAGEAL VARICES C. CHOLELITHIASIS D. ATROPHIC THYROID (5.2G) E. BILATERAL PITTING EDEMA FINAL CAUSE OF DEATH CIRRHOSIS AND CORONARY ARTERIOSCLEROSIS WITH ACUTE AND PRE-EXISTING MYOCARDIAL INFARCT FINAL NOTE This is a ___year old Hispanic female with a medical history significant for end stage liver disease, cryptogenic cirrhosis, esophageal varices, hypothyroidism, CKD, and DM. The patient presented on __/__/____ with nausea, vomiting, and poor oral intake. She subsequently developed hepatic encephalopathy and was transferred to the ICU. She also developed pneumonia which grew MRSA on sputum culture. The patient went into septic shock and became hypotensive and was maxed on pressors. She was able to be volume resuscitated and had improvement. She was transitioned to comfort care. The patient was pronounced dead on __/__/____ at __: __ PM. The family requested on autopsy to be performed following her death. At autopsy, the skin was jaundiced and there was scleral icterus noted in the eyes. The lungs were noted to have consolidation bilaterally. The liver appeared nodular and cirrhotic. The spleen was enlarged at 390g. There were choleliths noted within the gallbladder. The thyroid was atrophic at 5.2g. On microscopic examination, there was myocardial hypertrophy noted in the myocardium. There were also changes noted in the myocardium indicating acute and old myocardial infarct. The coronary arteries were arteriosclerotic. In the lungs, there was microscopic evidence of pulmonary hypertension, and diffuse alveolar damage with hyaline membranes. There were also emphysematous and anthracotic changes noted. The liver displayed evidence of nodular cirrhosis with a regenerative nodule. There was microscopic steatosis and lobular inflammation. There was hemosiderin deposition noted within the liver and pancreas sections. The kidneys appeared nephrosclerotic which was confirmed by a PAS stain. There was also evidence of chronic urocystitis noted within the bladder. There was dilatation of blood vessels noted in the esophagus indicative of varices. The cause of death in this case was cirrhosis and coronary arteriosclerosis. There are numerous causes of liver disease that can result in cirrhosis, either by causing chronic hepatic inflammation or cholestasis. The two most common causes of cirrhosis in the United States are alcoholic liver disease and hepatitis C. The clinical manifestations of cirrhosis may include nonspecific symptoms (e.g., anorexia, weight loss, weakness, fatigue) or signs and symptoms of hepatic decompensation (jaundice, pruritus, signs of upper gastrointestinal bleeding, abdominal distension from ascites, confusion due to hepatic encephalopathy). Physical examination findings may include jaundice, spider angiomas, gynecomastia, ascites, splenomegaly, palmar erythema, digital clubbing, and asterixis. Laboratory abnormalities may include elevated serum bilirubin, abnormal aminotransferases, elevated alkaline phosphatase/gamma-glutamyl transpeptidase, a prolonged prothrombin time/elevated international normalized ratio (INR), hyponatremia, and thrombocytopenia. In patients suspected of having cirrhosis, abdominal imaging is typically obtained, though radiographic imaging alone is not adequately sensitive or specific to diagnose cirrhosis. The findings must be viewed considering other signs of cirrhosis such as physical examination or laboratory test findings. A liver biopsy is required to definitively confirm the diagnosis of cirrhosis. However, it is generally not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and the results would not alter the patient's management. Determining the etiology of cirrhosis is important because it may influence treatment decisions, permit counseling of family members, and help predict the patient's prognosis. The initial evaluation includes obtaining a history, performing a physical examination, and obtaining routine blood tests (i.e., liver biochemical and function tests and a complete blood count). The findings from the initial evaluation are then used to guide additional testing. In this particular case, the cause of death was liver failure due to cirrhosis. Unfortunately for this patient, knowing the etiology of the cirrhosis may not have improved the prognosis because of the extent of the cirrhosis. Coronary arteriosclerosis also played a role in the cause of death by causing infarct within the myocardium. REFERENCES 1. Goldberg E, Chopra S. Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis. In: UpToDate, Runyon, B (Ed). Retrieved from http://www.uptodate.com/home2. Friedman, S. Clinical manifestations and diagnosis of alcoholic fatty liver disease and alcoholic cirrhosis. In: UpToDate, Runyon, B (Ed). Retrieved from http://www.uptodate.com/home 3. O'Shea RS, Dasarathy S, McCullough AJ, et al. Alcoholic liver disease. Hepatology 2010; 51:307. 4. Heidelbaugh JJ, Bruderly M. Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation. Am Fam Physician 2006; 74:756.

FINAL ANATOMIC DIAGNOSIS I. HEPATOBILIARY A. WELL-DIFFERENTIATED HEPATOCELLULAR CARCINOMA, RIGHT LOBE (3.1CM) B. CIRRHOSIS WITH BILE STASIS C. JAUNDICE AND SCLERAL ICTERUS D. ASCITES (1100 CC) FINAL CAUSE OF DEATH END STAGE LIVER CIRRHOSIS ASSOCIATED WITH HEPATITS B AND D FINAL NOTE This is a ___year old male with a history significant for ESLD (secondary to Hepatitis B and D), Hepatitis C, and EtOH/substance abuse. The patient was admitted for hepatic encephalopathy, but it was discovered that the patient had esophageal varices that bled during his inpatient stay. Bands were placed and the patient was hypotensive requiring fluid resuscitation and blood products. He developed lactic acidosis and the patient’s pH declined despite replacing bicarb. The patient was made comfort measures only and became hypotensive and bradycardic. The patient went into asystole and was pronounced dead on __/__/____ at __: __ PM and consent for a limited autopsy was obtained. At autopsy, there was significant jaundice and scleral icterus noted. The liver and gallbladder were removed with minimal incisions for examination. The liver was green, firm, and nodular. Sectioning of the liver revealed a 3.1cm mass located within the anterior lower right lobe. The mass appeared well circumscribed, soft, and green. Microscopically, the liver had extensive fibrosis, bile stasis, and bile duct proliferation, indicating cirrhosis. The mass was histologically consistent with a well-differentiated hepatocellular carcinoma. There was no evidence of malignancy within the gallbladder or the representative lymph nodes that were examined. There are numerous causes of liver disease that can result in cirrhosis, either by causing chronic hepatic inflammation or cholestasis. The two most common causes of cirrhosis in the United States are alcoholic liver disease and hepatitis C. The clinical manifestations of cirrhosis may include nonspecific symptoms (eg, anorexia, weight loss, weakness, fatigue) or signs and symptoms of hepatic decompensation (jaundice, pruritus, signs of upper gastrointestinal bleeding, abdominal distension from ascites, confusion due to hepatic encephalopathy). Physical examination findings may include jaundice, spider angiomas, gynecomastia, ascites, splenomegaly, palmar erythema, digital clubbing, and asterixis. Laboratory abnormalities may include elevated serum bilirubin, abnormal aminotransferases, elevated alkaline phosphatase/gamma-glutamyl transpeptidase, a prolonged prothrombin time/elevated international normalized ratio (INR), hyponatremia, and thrombocytopenia. In patients suspected of having cirrhosis, abdominal imaging is typically obtained, though radiographic imaging alone is not adequately sensitive or specific to diagnose cirrhosis. The findings must be viewed considering other signs of cirrhosis such as physical examination or laboratory test findings. A liver biopsy is required to definitively confirm the diagnosis of cirrhosis. However, it is generally not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and the results would not alter the patient's management. Determining the etiology of cirrhosis is important because it may influence treatment decisions, permit counseling of family members, and help predict the patient's prognosis. Hepatitis B virus (HBV) infection is a global public health problem. The spectrum of clinical manifestations of HBV infection varies in both acute and chronic disease. During the acute phase, manifestations range from subclinical hepatitis to anicteric hepatitis, icteric hepatitis, and fulminant hepatitis; during the chronic phase, manifestations range from an asymptomatic carrier state to chronic hepatitis, cirrhosis, and hepatocellular carcinoma. The clinical outcome of HBV infection depends upon the age at infection, the level of HBV replication, and the immune status of the host. Hepatitis D is caused by a defective virus: the hepatitis D virus (HDV). HDV is often referred to as hepatitis delta virus or delta agent. However, the term HDV is preferred. HDV infection is closely associated with hepatitis B virus (HBV) infection. Although HDV can replicate autonomously, the simultaneous presence of HBV is required for complete virion assembly and secretion. As a result, individuals with hepatitis D are always dually infected with HDV and HBV. Due to interference mechanisms that are not well understood, HBV replication is suppressed in most HDV-infected individuals. In the Western world, where the predominant genotype is genotype I, acute hepatitis D has an increased risk of a fulminant course when compared to acute hepatitis B. Once chronic HDV infection is established, it usually exacerbates the preexisting liver disease due to HBV. Progression towards cirrhosis may be rapid. HDV-associated chronic liver disease may also run an indolent course and asymptomatic HDV carriers have been found in some geographical areas. Whether superimposed HDV infection accelerates the development of hepatocellular carcinoma in patients with HBsAg-positive cirrhosis is controversial. REFERENCES 1. Goldberg E, Chopra S. Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis. In: UpToDate, Runyon, B (Ed). Retrieved from http://www.uptodate.com/home 2. Friedman, S. Clinical manifestations and diagnosis of alcoholic fatty liver disease and alcoholic cirrhosis. In: UpToDate, Runyon, B (Ed). Retrieved from http://www.uptodate.com/home 3. Lok, A. Characteristics of the hepatitis B virus and pathogenesis of infection. In: UpToDate, Esteban, R (Ed). Retrieved from http://www.uptodate.com/home 4. O'Shea RS, Dasarathy S, McCullough AJ, et al. Alcoholic liver disease. Hepatology 2010; 51:307. 5. Heidelbaugh JJ, Bruderly M. Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation. Am Fam Physician 2006; 74:756. 6. Lok, A. Pathogenesis, epidemiology, natural history, and clinical manifestations of hepatitis D virus infection. In: UpToDate, Esteban, R (Ed). Retrieved from http://www.uptodate.com/home

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. CARDIOMEGALY WITH FOUR CHAMBER HYPERTROPHY (710G) B. ACUTE MYOCARDIAL INFARCT II. RESPIRATORY A. BILATERAL PULMONARY THROMBOEMBOLISM B. PULMONARY INFARCT III. OTHER A. MORBID OBESITY (500LBS) B. HIRSUTISM FINAL CAUSE OF DEATH PULMONARY THROMBOEMBOLISM DUE TO MORBID OBESITY; ACUTE MYOCARDIAL INFARCT FINAL NOTE This is a __year old female with a history significant for morbid obesity and recent pneumonia who presented with dyspnea. She was admitted for bilateral pulmonary embolism seen on CT angiogram. The patient decompensated after intubation awaiting catheter procedure to deliver lytics for the emboli. The patient was pronounced dead on __/__/___ at __: __ and consent for an autopsy was obtained. At the time of autopsy, it was noted that the heart was enlarged at 710 grams, with hypertrophied muscle fibers and evidence of acute infarct on microscopy. There was some mild atherosclerotic change within the coronary arteries. Examination of the lungs demonstrated large, bilateral pulmonary emboli within the arteries. There was evidence of old organized thrombi and fresh thromboemboli. The remaining lung parenchyma showed some evidence of infarct microscopically that were associated with the thromboemboli. No underlying malignancy (a possible cause of hypercoagulable state) was identified in the organs examined but cannot be excluded due to the limited nature of the autopsy. Most of the pathology in this case rested within the heart and lungs in the form of pulmonary thromboemboli and acute myocardial infarct. Acute pulmonary embolism (PE) is a common disease with mortality rate as high as 30% if left untreated (1). Prompt diagnosis and treatment can reduce mortality, but the presenting symptoms are often nonspecific and vague. A massive pulmonary embolus is defined by a systolic blood pressure <90mmHg or a drop in systolic blood pressure by >40mmHg for greater than 15 minutes (1). Index of suspicion should be high any time there is hypotension with elevated central venous pressure not explained by other entities. Massive pulmonary embolism is a high-mortality event which can result in right ventricular failure and sudden death (1). Incidence of pulmonary embolism is hard to quantitate because more than half of all pulmonary emboli probably go undiagnosed; one study examined 42 million deaths over a 20-year period and found that approximately 600,000 had been diagnosed with PE and of these, 200,000 had PE as cause of death (approximately 0.47%) (1). The incidence is expected to rise with the utilization of computed tomographic pulmonary angiography (CT-PA). There are multiple factors involved in determining the prognosis of PE. Right ventricular dysfunction, right ventricular thrombus, deep vein thrombosis, elevated brain natriuretic peptide, elevated serum troponin, hyponatremia, and elevated lactate levels are all associated with increased mortality (1). The Pulmonary Embolism Severity Index (PESI) and the Simplified Pulmonary Embolism Severity Index (sPESI) are prognostic models utilized to stratify patients for thrombolytic therapy based on their risk factors and symptoms. Most pulmonary thromboemboli originate in the deep venous system of the lower extremities, especially the iliofemoral veins; right heart, pelvic, renal, and upper extremity veins are less common sites of origin (1). Most pulmonary emboli are multiple with predilection for lower lobes. Hypotension manifests when cardiac output is reduced by increased pulmonary vascular resistance; eventually the right ventricle is unable to overcome the increased pressure and cannot maintain pulmonary perfusion (1). There are many well-recognized risk factors for pulmonary embolism. Immobilization, surgery (within 3 months), stroke, paralysis, central venous instrumentation (within 3 months), malignancy, chronic heart disease, autoimmune disease, and a history of venous thromboembolism all increased risk of pulmonary embolism (1). In addition, women who are obese (BMI ≥29), heavy cigarette smokers (>25 cigarettes/day), and hypertensive are at an even greater risk (1). A 1992 chronobiological study out of Italy examined 507 consecutive sudden deaths that occurred outside the hospital; at autopsy 48 of them were found to have fatal pulmonary emboli and of these patients, circadian and circannual rhythmicity showed statistically significant predilection for morning and winter (2). The Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) looked at 824 patients without underlying cardiopulmonary disease and determined that the most common presenting symptoms of PE are dyspnea, pleuritic pain, cough, >2 pillow orthopnea, calf or thigh pain, calf or thigh swelling, and wheezing; the most common signs are tachypnea, tachycardia, rales, decreased breath sounds, accentuated pulmonic component of the second heart sound, and jugular venous distension (3). However, pulmonary embolism is frequently asymptomatic as demonstrated by a review of 5233 patients with deep vein thrombosis, 32% of which had asymptomatic PE (1). When symptoms are present, shock or hypotension is the principal prognostic marker and indicates a high-risk of death (30-50%) (1). The patient in this case appears to have suffered multiple pulmonary emboli varying in age. Internal examination revealed multiple large bilateral thromboemboli. Microscopic examination demonstrated multiple bilateral thrombi and thromboemboli that varied in age, which indicates that the patient has had pulmonary emboli prior to presentation. The unexpected sudden death of the patient in this case is explained by pulmonary thromboembolism which was associated with morbid obesity and acute myocardial infarct. (1)Thompson, T., and Hales, C., "Overview of Acute Pulmonary Embolism". UpToDate. Jul 2014. (2)Gallerani, M., et al "Sudden Death from Pulmonary Thromboembolism: Chronobiological Aspects". Eur Heart J. 1992: 13(5):661-665. (3)Stein, P., et al "Multidetector Computer Tomography for Acute Pulmonary Embolism". NEJM. 2006:354(22):2317-2327.

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. MYOCARDIAL HYPERTROPHY B. MILD CORONARY ARTERIOSCLEROSIS (LAD 20%, LCX 20%, RCA 15%) II. RESPIRATORY A. ORGANIZING PNEUMONIA, RIGHT LUNG B. ALVEOLAR HEMORRHAGE C. PULMONARY EDEMA (R: 700G, L: 470G) D. EMPHYSEMATOUS CHANGES III. HEPATOBILIARY A. MICRONODULAR CIRRHOSIS WITH LOBULAR INFLAMMATION B. ASCITES (3200CC) IV. GENITOURINARY A. BILATERAL NEPHROSCLEROSIS WITH DIABETIC CHANGES B. TUBULAR NECROSIS IV. OTHER A. ATROPHIC THYROID (7.9G) B. S/P HYSTERECTOMY AND BILATERAL SALPINGO-OOPHERECTOMY C. S/P CHOLECYSTECTOMY FINAL CAUSE OF DEATH COMPLICATIONS OF CIRRHOSIS WITH ASSOCIATED HEPATORENAL SYNDROME FINAL NOTE This is a __ year old Hispanic female with a medical history pertinent for autoimmune hepatitis, cirrhosis, hypothyroidism, diabetes, asthma, and hypertension who presented to ____Hospital on __/__/____ complaining of shortness of breath. Her shortness of breath worsened during her stay, and she developed acute kidney injury that was consistent with a hepatorenal syndrome. The patient developed hyperkalemia which was refractory to treatment. The patient did not improve clinically and was made comfort measures on __/__/___. The patient went into asystole and was pronounced dead at __: __ pm on __/__/___. An autopsy was requested by the family. At autopsy, the heart was found to be enlarged at 400g. The lungs were noted to have edema bilaterally. The liver appeared micronodular and cirrhotic. There was 3200cc of ascites within the peritoneum. The kidneys were nephrosclerotic with the right weighing 148 grams and the left weighing 116 grams. The thyroid was atrophic at 7.9g. On microscopic examination, there was myocardial hypertrophy noted in the myocardium. There was also some minimal interstitial and perivascular fibrosis. In the lungs, there was microscopic evidence of some organizing pneumonia, and alveolar hemorrhage. There were also emphysematous changes noted. The liver displayed evidence of micronodular cirrhosis with lobular inflammation, but no steatosis. The kidneys appeared nephrosclerotic with nodular glomeruli which was confirmed by a PAS stain. There was also evidence of tubular necrosis. The cause of death in this case was complications of cirrhosis with associated hepatorenal syndrome. There are numerous causes of liver disease that can result in cirrhosis, either by causing chronic hepatic inflammation or cholestasis. The two most common causes of cirrhosis in the United States are alcoholic liver disease and hepatitis C. The clinical manifestations of cirrhosis may include nonspecific symptoms (e.g., anorexia, weight loss, weakness, fatigue) or signs and symptoms of hepatic decompensation (jaundice, pruritus, signs of upper gastrointestinal bleeding, abdominal distension from ascites, confusion due to hepatic encephalopathy). Physical examination findings may include jaundice, spider angiomas, gynecomastia, ascites, splenomegaly, palmar erythema, digital clubbing, and asterixis. Laboratory abnormalities may include elevated serum bilirubin, abnormal aminotransferases, elevated alkaline phosphatase/gamma-glutamyl transpeptidase, a prolonged prothrombin time/elevated international normalized ratio (INR), hyponatremia, and thrombocytopenia. In patients suspected of having cirrhosis, abdominal imaging is typically obtained, though radiographic imaging alone is not adequately sensitive or specific to diagnose cirrhosis. The findings must be viewed considering other signs of cirrhosis such as physical examination or laboratory test findings. A liver biopsy is required to definitively confirm the diagnosis of cirrhosis. However, it is generally not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and the results would not alter the patient's management. Determining the etiology of cirrhosis is important because it may influence treatment decisions, permit counseling of family members, and help predict the patient's prognosis. The initial evaluation includes obtaining a history, performing a physical examination, and obtaining routine blood tests (i.e., liver biochemical and function tests and a complete blood count). The findings from the initial evaluation are then used to guide additional testing. Autoimmune hepatitis is a chronic hepatitis characterized by immunologic and autoimmunologic features, generally including the presence of circulating autoantibodies and a high serum globulin concentration. Autoimmune hepatitis has a heterogeneous and fluctuating nature, leading to marked variability in its clinical manifestations. Its spectrum ranges from asymptomatic patients to those with considerable and sometimes debilitating symptoms, and even those with acute liver failure. Diagnosis is based upon characteristic serologic and histologic findings and exclusion of other forms of chronic liver disease. It can often be strongly suspected based upon clinical and laboratory features, and thus a liver biopsy may not always be necessary in patients with typical findings on noninvasive testing In this particular case, the cause of death was liver failure due to cirrhosis. The extensive cirrhosis caused the patient to develop hepatorenal syndrome which contributed to the cause of death. REFERENCES 1. Goldberg E, Chopra S. Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis. In: UpToDate, Runyon, B (Ed). Retrieved from http://www.uptodate.com/home2. Friedman, S. Clinical manifestations and diagnosis of alcoholic fatty liver disease and alcoholic cirrhosis. In: UpToDate, Runyon, B (Ed). Retrieved from http://www.uptodate.com/home 3. O'Shea RS, Dasarathy S, McCullough AJ, et al. Alcoholic liver disease. Hepatology 2010; 51:307. 4. Heidelbaugh JJ, Bruderly M. Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation. Am Fam Physician 2006; 74:756. 5. Krawitt EL. Autoimmune hepatitis. N Engl J Med 2006; 354:54

FINAL ANATOMIC DIAGNOSIS I. CARDIOVASCULAR A. MYOCARDIAL HYPERTROPHY (380G, L VENTRICLE: 1.7CM) B. SEVERE CORONARY ARTERIOSCLEROSIS (LAD: 75%, LCX: 75%, RCA: 60%) C. S/P STENT PLACEMENT IN RIGHT CORONARY ARTERY II. RESPIRATORY A. EARLY BRONCHOPNEUMONIA B. PLEURAL EFFUSION (R: 500CC, L: 600CC) C. PULMONARY EDEMA AND CONGESTION (R: 810G, L: 1050G) III. HEPATOBILIARY A. NUMEROUS FIBRIN THROMBI B. CENTRILOBULAR CONGESTION, CENTRAL VENULITIS, AND LOBULAR HEPATITIS IV. GENITOURINARY A. NEPHROSCLEROTIC CHANGES, BILATERAL (R: 175G, L: 190G) B. FIBRIN THROMBI V. OTHER A. S/P SPLENECTOMY AND DISTAL PANCREATECTOMY B. ANTEMORTEM BLOOD CULTURES POSITIVE FOR STREPTICOCCUS PNEUMONIAE FINAL CAUSE OF DEATH HEART FAILURE SECONDARY TO SEPSIS WITH ASSOCIATED DISSEMINATED INTRAVASCULAR COAGULATION FINAL NOTE This is a __ year old male with a medical history significant for CAD/MI with stent placement in ____, splenectomy and distal pancreatectomy due to trauma, and left hip replacement that presented to the ED complaining of chills, shaking, and fever. The patient worked as a teacher and started to have shaking while at work. The patient decided to go to the ER when he started feeling lethargic and dizzy. He was found to have a fever, dry cough, and headache, but denied neck stiffness, photophobia, chest pain, shortness of breath, or diarrhea. The patient had a systolic blood pressure of 115 at presentation, but quickly became hypotensive with a blood pressure of 80/50. The patient was admitted to the ICU but continued to decompensate despite medical intervention within 12 hours of admission. The patient was pronounced dead at __: __ on __/__/____ and consent for an autopsy with no limitations was obtained. At autopsy, the patient was found to have red and blotchy skin. There was evidence of myocardial hypertrophy and severe coronary arteriosclerosis with the LAD having 75% occlusion. A stent was seen in the RCA. There was pleural effusion noted and the lungs were edematous. Microscopically there was evidence of early bronchopneumonia. In the liver there were numerous fibrin thrombi noted as well as centrilobular congestion, central venulitis and lobular hepatitis. In the kidneys, nephrosclerotic changes were seen as well as more fibrin thrombi. It was noted that antemortem blood cultures were positive for streptococcus pneumoniae. The cause of death in this case was heart failure secondary to sepsis with associated DIC. Asplenic individuals are at increased risk for overwhelming sepsis, a fulminant and rapidly fatal illness that complicates bacteremic infections due to encapsulated pathogens, which are normally cleared from the circulation by the spleen. Fulminant sepsis in asplenic patients is classically caused by encapsulated organisms, including Streptococcus pneumoniae, Hemophilus influenzae, and Neisseria meningitidis. The single most important pathogen is Streptococcus pneumoniae. In a review of 349 episodes of sepsis in patients with anatomic or functional asplenia, S. pneumoniae accounted for 57 percent of infections and 59 percent of deaths. Fulminant asplenic sepsis may follow minor upper or lower respiratory tract symptoms but also can develop precipitously without antecedent complaints. The illness provokes acute onset of extreme malaise, intractable rigors, high fever, and rapidly manifests complications of high-grade bacteremia that can include petechiae, purpura, meningitis, and hypotension. Fever or rigors should be considered the first warning signs of possible sepsis in asplenic patients. Broad-spectrum antibiotics must be initiated promptly since clinical deterioration can occur over hours. Antibiotic administration should not be delayed by a diagnostic workup. This patient had a recent history of myocardial infarction, and asplenia due to trauma at a young age. Due to this, the patient had a susceptibility to encapsulated organisms, specifically S. pneumonia. The patient became septic and developed DIC, which likely strained an already compromised heart. This may explain the quick clinical course that the patient had. References: 1. Pasternack, M. Clinical features and management of sepsis in the asplenic patient. Weller, P (Ed.). UpToDate.com. 2. Rubin LG, Schaffner W. Clinical practice. Care of the asplenic patient. N Engl J Med 2014; 371:349. 3. Schwartz PE, Sterioff S, Mucha P, et al. Postsplenectomy sepsis and mortality in adults. JAMA 1982; 248:2279. 4. Gopal V, Bisno AL. Fulminant pneumococcal infections in 'normal' asplenic hosts. Arch Intern Med 1977; 137:1526.

CLINICAL SUMMARY 15-DAY-OLD MALE INFANT (WEIGHT: 1620 GM; EXPECTED: 949 +/- 190 G), BORN PREMATURELY TO A __-YEAR-OLD G1P0 DELIVERED BY NORMAL SPONTANEOUS VAGINAL DELIVERY AFTER PRETERM PREMATURE RUPTURE OF MEMBRANES. UPON DELIVERY, THE INFANT WENT INTO RESPIRATORY DISTRESS, REQUIRING CHRONIC RESPIRATORY SUPPORT. THE BABY WAS STARTED ON TOTAL PARENTERAL NUTRITION. ON __/__/___, THE INFANT DEVELOPED SIGNS OF NEONATAL SEPSIS AND EXPIRED ON __/__/____ FROM MULTI-ORGAN DYSFUNCTION. CONSENT FOR COMPLETE AUTOPSY WAS OBTAINED. PROVISIONAL ANATOMIC DIAGNOSIS CULTURES OF BLOOD, CEREBRAL SPINAL FLUID, AND LUNG TISSUE POSITIVE FOR PSEUDOMONAS AERUGINOSA RESPIRATORY SYSTEM: PETECHIAL HEMORRHAGE, BILATERAL LUNGS CARDIOVASCULAR PATENT FORAMEN OVALE PATENT DUCTUS ARTERIOSUS NO CARDIAC ANOMALIES HEPATOMEGALY CENTRAL NERVOUS SYSTEM INTRACRANIAL HEMORRHAGE BRAIN FIXED IN FORMALIN FOR SUBSEQUENT DETAILED NEUROLOGIC EXAMINATION SKIN SENT FOR CYTOGENETIC EVALUATION: PENDING NO CONGENITAL ANOMALIES OF MAJOR ORGANS. NO DYSMORPHIC FEATURES. PLACENTA: ACUTE CHORIOAMNIONITIS PERMISSION, TIME, AND EXTENT Permission for a full autopsy, without restrictions, was obtained from the MOTHER on __/__/____. The autopsy was performed at ____ Hospital on __/__/____ at __: __am, approximately 20 hours postmortem. MEASUREMENTS: Actual (expected). Expected measurements are for a 29-week gestation fetus Crown-rump length: 29.5 cm (25.9 +/- 2.8 cm) Crown-heel length: 42.0 cm (35.6 +/- 4.4 cm) Foot length: 5.8 cm (5.4 +/- 0.8 cm) Hand length: 4.6 cm Head circumference: 26.7cm Chest circumference: 25.7 cm Abdomen circumference: 30.1 cm Outer canthal: 6.2 cm Inner canthal: 1.9 cm Intermammary space: 6.5 cm Anterior fontanelle: 3.0 x 2.5cm Posterior fontanelle: 1.5 x 1.0 cm Lungs: 67 g (25.3 +/- 12.6 g) Heart: 15 g (7.2 +/- 2.7 g) Liver: 78 g (43.5 +/- 15.8 g) Spleen: 4.1 g (2.6 +/-0.9 g) Pancreas: 0.8 g (1.5 +/- 1.0 g) Thymus: 4.0 g (3.0 +/- 1.9 g) Adrenals: 5.1 g (3.0 +/- 1.2 g) Kidneys: 38.8 (10.9 +/- 4.4 g) Weight: 1620 g (1077 +/-449 g) External examination: The body is that of a 15-day old ex 26 3/7-week premature male infant. There is no livor mortis. Slight rigor mortis limited to the extremities is present. The skin is hyperemic, and no jaundice is visible. There is an area of erythema over the left cheek and the facial skin is dusky. The face has no dysmorphic features, and the scalp is covered by short black wavy hair. The head shows bitemporal narrowing. Cleft lip, cleft palate and short philtrum are absent. The nares are patent. The chest is symmetric. The abdomen is distended, and the liver is palpable. Both the upper and lower extremities are symmetrically developed. Five digits are present on each extremity and palmar creases are normal. There is minimal blue discoloration appreciated in the fingertips. The anus is probe patent. The external genitalia are consistent with an uncircumcised male. The umbilicus is healed. The following medical paraphernalia are identified: central line. Internal examination: The body is opened with a U- shaped incision. The panniculus layer is 0.3cm thick. There is serosanguineous free fluid along the pleural and peritoneal cavities with the following accumulations: right pleural 20cc, left pleural 20cc and peritoneal 5cc. The diaphragm is intact, and no herniation of the abdominal organs is appreciated. The esophagus, stomach, small intestine, appendix, large intestine, liver, pancreas, ureters, testes, and kidneys are found in normal anatomical position. Neck: No petechial hemorrhages are seen in the thymus. The trachea is probe patent. No ulcerations or tracheo-esophageal fistulas are present. Thorax: The lungs show diffuse areas of petechial hemorrhage and are moderately congested. The left upper lobe and left lower lobe show several white rimmed circular lesions ranging from 0.1 – 0.2 cm in greatest dimension along the oblique fissure. The heart has four chambers, normal valves, a patent foramen ovale and a patent ductus arteriosus. No petechial hemorrhages are seen in the heart. Abdomen: The spleen is congested and dark red with smooth surface. The liver is large, congested, and dark red to brown with a smooth surface. A 0.8 x 0.7 cm subcapsular hematoma is identified on the anterior inferior surface of the right lobe. There is no malrotation present and the stomach communicates proximally with the esophagus and distally with the small intestine. The gastroesophageal junction is well defined. The appendix is intact, tan in color and located in the correct anatomical position. The small and large bowel contains soft green stool and show no mucosal lesions, adhesions, or strictures. Retroperitoneum: The kidneys are tan, brown, congested, and have a normal shape. Bivalving of both kidneys reveals no obstruction of the pelvis-calyceal system and bilateral ureters show patent lumen directly communicating with the bladder. The adrenal glands are congested. Brain: The anterior and posterior fontanelles are open. The brain shows a large area of hemorrhage over the right occipital and right temporal lobe. Microscopic Description: Cardiovascular system (1A-1C): Sections of the myocardium and papillary muscle show no evidence of vasculitis, thrombosis, calcifications, or inflammation. No viral inclusions are identified, with negative immunoreactivity for cytomegalovirus. Respiratory system (1D-1H): Sections of the lungs show late canalicular/early saccular stage, consistent with gestational age. There is moderate congestion with residual hyaline membranes and dilatation of the alveolar spaces with patchy areas of necrosis and hemorrhage. Numerous intraalveolar macrophages are seen. Trichrome stain highlights moderate intraalveolar fibrosis. Gram stain highlights gram negative rods throughout the alveoli and invading the intima of arteries, consistent with vasculitis. Liver (1K): The liver is congested with focal areas of hemorrhage and necrosis. Small areas of residual extramedullary hematopoiesis are identified. Viral cytopathic changes, necrosis, thrombosis, and vasculitis are not seen. Spleen (1L): The spleen is congested and focally hemorrhagic. Thymus (1L): The thymus shows mild lymphocyte depletion GI Tract (1I-1J): Sections of the stomach, GE junction, and small intestine show congestion. No hemorrhage, infarct, necrosis, or vasculitis is seen. Ganglion cells are identified. Endocrine (1L-1N): Sections show thyroid follicles appropriate for gestational age with focal brown fat. The pancreas shows unremarkable islets and acini. The adrenal glands show congestion and microcystic change. No hemorrhage, necrosis, or vasculitis is identified. Genitourinary (1O-R): Sections of the bladder show autolysis of the urothelium. The prostate, right and left testes are histologically identified. Sections of the testes show congestion. The kidneys show congestion of corticomedullary junctions without evidence of vasculitis, hemorrhage, or necrosis. Muscle (1S): Sections of muscle are unremarkable. Trachea (1T): Section of the trachea show ulceration with normal cartilage. Bone (1U): The costochondral junction shows normal cartilage and bone with normocellular trilineage hematopoiesis. Gram stain for bacteria is negative. Summary of Sections: 1A: RIGHT VENTRICLE AND RIGHT ATRIUM 1B: LEFT VENTRICLE AND LEFT ATRIUM 1C: LEFT PAPILLARY MUSCLE 1D: RUL 1E: RML 1F: RLL 1G: LUL (WITH LESIONS) 1H: LLL (WITH LESIONS) 1I: GE JUNCTION/STOMACH 1J: RECTUM, APPENDIX, ILEOCECAL VALVE, SMALL INTESTINE, LARGE INTESTINE 1K: LIVER 1L: SPLEEN, PANCREAS, THYMUS 1M: LEFT ADRENAL 1N: RIGHT ADRENAL 1O: LEFT AND RIGHT KIDNEY 1P: PROSTATE AND BLADDER 1Q: LEFT TESTES 1R: RIGHT TESTES 1S: MUSCLE 1T: TRACHEA 1U: COSTOCHONDRAL JUNCTION 1V: THYROID FINAL NOTE This was a ___day old male infant born prematurely at 26 weeks gestation to a __ year old GIP0 mother by normal spontaneous delivery after preterm premature rupture of membranes. Upon delivery, the infant went into respiratory distress, requiring chronic respiratory support. The baby was started on total parenteral nutrition. On __/__/___, the infant developed signs of neonatal sepsis and expired on __/__/___ from multi-organ dysfunction. Consent for complete autopsy was obtained. At autopsy, the baby showed no congenital anomalies or dysmorphic features. The lungs were moderately congested with several white rimmed circular lesions and diffuse areas of petechial hemorrhage. Multiple organs, including the spleen, liver, and adrenal glands were congested. The brain showed a large area of subarachnoid hemorrhage over the right frontal lobe and cerebellum. On microscopic examination, the lung development was consistent with gestational age. There were patchy areas of necrosis and hemorrhage, vasculitis, residual hyaline membranes, and dilatation of the alveolar spaces. A gram stain of the lung tissue confirmed the presence of gram-negative rods throughout the alveoli and invading the intima of arteries. The liver was congested with areas of hemorrhage and necrosis without evidence of vasculitis. A gram stain of the bone did not reveal evidence of osteomyelitis. Furthermore, neuropathologic evaluation did not reveal evidence of meningitis or meningoencephalitis. Ante-mortem cultures from the blood (peripheral and Broviac line) and respiratory cultures were positive for Pseudomonas aeruginosa, as were postmortem cultures from blood, cerebral spinal fluid, and lung tissue. Sepsis due to hematogenous spread of Pseudomonas aeruginosa from underlying pneumonia was the most likely cause of death in this case. Hospital acquired pneumonia (HAP) is a pulmonary infection that develops in patients hospitalized for more than 48 hours, either in the ICU or other wards. Ventilator associated pneumonia (VAP) is a subset of HAP that occurs in mechanically ventilated patients more than 48 hours after tracheal intubation and is the most frequent ventilator associated complication, occurring in 9-40% of intubated patients. P. Aeruginosa is the most widespread multidrug-resistant gram-negative pathogen causing pneumonia in hospitalized patients and carries the highest mortality among hospital acquired infections. Infection can occur via aspiration of endogenous oral flora or via aspiration of organisms from contamination of ventilator tubing or other healthcare devices. Acute P. aeruginosa pneumonia is usually characterized by cough productive of purulent sputum, dyspnea, fever, chills, confusion, and severe systemic toxicity. Patients with ventilator-associated P. aeruginosa pneumonia may also present with increased tracheobronchial secretions and decreased ventilator performance, which can develop suddenly or gradually. These infections present as severe sepsis or septic shock with respiratory dysfunction and or multi-organ dysfunction due to the pathogen’s ability to invade tissues. Histopathologic changes in patients with pneumonia due to P. aeruginosa typically include microabscesses with focal hemorrhage and necrosis of the alveolar septae without evidence of bacterial invasion of vessel walls or vascular necrosis. REFERENCES Barbier F, Andremont A, Wolff M, Bouadma L. Hospital-acquired pneumonia andventilator-associated pneumonia: recent advances in epidemiology and management.Curr Opin Pulm Med. 2013 May;19(3):216-28 Rello J, Lisboa T, Koulenti D. Respiratory infections in patients undergoing mechanical ventilation. Lancet Respir Med. 2014 Aug 20

Final anatomic diagnosis I. CLINICAL SUMMARY TWO-DAY OLD MALE NEONATE BORN AT TERM (WEIGHT: 2990 G, EXPECTED: 2922 +/- 450 G); PRENATAL DIAGNOSIS OF COMPLEX CONGENTIAL HEART DISEASE. TWO DAYS AFTER BIRTH, THE BABY HAD SUDDEN CARDIAC ARRHYTHMIA AND 30 MINUTES LATER WAS PRONOUNCED DEAD AT __: __ AM ON __/__/___. CONSENT FOR AUTOPSY LIMITED TO CHEST AND ABDOMEN WAS OBTAINED. II. EARLY NEONATAL DEATH ASSOCIATED WITH COMPLEX CONGENITAL HEART DISEASE CHARACTERIZED BY: A. CARDIOMEGALY (50.1 G, EXPECTED: 17 G). B. BIVENTRICULAR AND SEPTAL HYPERTROPHY (RIGHT VENTRICLE: 0.4 CM, LEFT VENTRICLE: 1.2 CM). C. ATRIAL SEPTAL DEFECT, 0.6 CM. D. SUBAORTIC OUTFLOW STENOSIS. E. CLEFT MITRAL VALVE. F. PATENT DUCTUS ARTERIOSUS. G. UNREMARKABLE TRICUSPID VALVE, PULMONARY VALVE AND AORTIC ARCH. III. RESPIRATORY SYSTEM: A. ABNORMAL LUNG LOBATION, BILATERAL: 1. TWO LOBES, RIGHT LUNG. 2. SINGLE LOBE, LEFT LUNG. B. EARLY ACUTE PNEUMONIA, BILATERAL. IV. OTHER: A. CONGESTIVE HEPATOSPLENOMEGALY (LIVER: 219.2 G, EXPECTED: 78 G; SPLEEN: 14.1 G, EXPECTED: 8 G). V. NO CONGENITAL ANOMALIES OF KIDNEYS, GI TRACT, LIVER. VI. ANCILLARY STUDIES: A. ANTEMORTEM BLOOD SENT FOR KARYOTYPING: 46 XY, NORMAL MALE KARYOTYPE. B. LUNG TISSUE AND BLOOD SENT FOR MICROBIOLOGIC STUDIES: NEGATIVE. FINAL CAUSE OF DEATH CONGENITAL HYPERTROPHIC CARDIOMYOPATHY INCOMPATIBLE WITH LIFE FINAL NOTE This is a case of a 39 week and __days old female (weight 2990 gm) who was born on __/__/____. The baby had known complex congenital heart disease consisting of severe hypertrophic cardiomyopathy, partial atrioventricular canal, and severe mitral regurgitation. The baby required cpap but without additional oxygen. Ekg’s following birth showed ischemic changes. On __/__/____, the baby had sudden cardiac arrhythmia and 30 minutes later was pronounced dead at __: __ am. Consent for complete autopsy was obtained. At autopsy, there were no dysmorphic features noted on external examination. Upon internal examination, the heart was noted to be enlarged and weighing 50.1 grams. Grossly, there were multiple abnormalities within the heart noted including significant hypertrophy, ASD, subaortic outflow stenosis, and cleft mitral valve. Microscopically, there was no evidence of ischemia, calcifications, are viral cytopathic effects. The lungs appeared to have some petechial hemorrhage. On microscopic examination, there was evidence of an early acute bilateral pneumonia. There were no microscopic abnormalities within the remaining major organs. The ancillary studies for karyotyping showed a normal male karyotype and the lung tissue and blood cultures were both negative. The main pathology in this case was the congenital hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy (HCM) is defined by its wall thickening, hence the term hypertrophic heart disease. However, its major impact on human health is its predilection to be inherited, its reputation as a common cause of sudden death in young, healthy, athletic individuals, and its potential for heart failure. HCM is a primary myocardial disorder with an autosomal dominant pattern of inheritance that is characterized by hypertrophy of the left (± right) ventricle with histological features of myocyte hypertrophy, myofibrillar disarray, and interstitial fibrosis. HCM is one of the most common inherited cardiac disorders, with prevalence in young adults of 1 in 500. The clinical diagnosis of HCM is conventionally made by imaging with two-dimensional echocardiography. Subaortic obstruction in HCM represents true mechanical impedance to LV outflow, producing markedly increased intraventricular pressures that over time may be detrimental to LV function, probably by increasing myocardial wall stress and oxygen demand. One of the underlying causes considered in this case was Noonan syndrome. Noonan syndrome is an autosomal dominant, variably expressed, multisystem disorder with an estimated prevalence of 1 in 1000–2500. Noonan syndrome is the second most common syndromic cause of congenital heart disease, exceeded in prevalence only by trisomy 21. Several cardiovascular phenotypes occur in Noonan syndrome. The most common are pulmonary stenosis (often with dysplastic valves; 50–60%), hypertrophic cardiomyopathy (20%), and secundum atrial septal defect (6–10%), but ventricular septal defect, peripheral pulmonary stenosis, atrioventricular canal, aortic stenosis, mitral valve abnormalities, aortic coarctation, and coronary artery anomalies have also been noted. Hypertrophic cardiomyopathy can be mild or severe and can present from the prenatal period to late childhood. Almost 25% of patients die because of heart failure in the first year, although the rate of sudden death is lower than that for familial hypertrophic cardiomyopathy. Frequently, Noonan syndrome remains a clinical diagnosis and due to the variability in presentation and the need for a multidisciplinary approach, it is recommended that the entity is identified early and managed from a comprehensive standpoint. REFERENCES 1. Towbin J, Ware S, Jefferies J. Muscle: Fundamental Biology and Mechanisms of Disease, Chapter 33: Congenital Cardiomyopathies, 459-472 2. Maron B, Olivotto I. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 66: Hypertrophic Cardiomyopathy, 1574-1588 3. Romano A, et al. Noonan Syndrome: Clinical Features, Diagnosis, and Management Guidelines. Pediatrics: Journal of the American Academy of Pediatrics. Volume 126, Number 4, October 2010. 4. Roberts A, et Al. Noonan syndrome. The Lancet: Vol 381, January 2013 pages 333-342.

FINAL ANATOMIC DIAGNOSIS I. CLINICAL HISTORY: NINE-DAY OLD FEMALE NEONATE BORN AT TERM AT ___ HOSPITAL (WEIGHT: 3402 G, EXPECTED: 3163 +/- 595 G). POST-NATAL PROLONGED HOSPITALIZATION (5 DAYS) DUE TO ABO INCOMPATIBILITY REQUIRING PHOTOTHERAPY. THREE DAYS AFTER DISCHARGE, MOTHER PRESENTED TO ST. FRANCIS ED WITH INFANT SECONDARY TO MULTIPLE EPISODES OF PASSING STOOL, EMESIS, DECREASED FEEDING AND INCREASED SLEEP; BABY WAS FOUND ON PROFOUND METABOLIC ACIDOSIS, DIC AND MULTISYSTEM ORGAN FAILURE. SHE WAS TRANSFERRED TO CCMC NICU ON __/__/____ AND WAS PRONOUNCED DEAD AT __: __ PM ON THE SAME DAY. CONSENT FOR AUTOPSY LIMITED TO CHEST AND ABDOMEN WAS OBTAINED. II. NEONATAL DEATH ASSOCIATED WITH MULTIORGAN FAILURE AND DIC: A. HEPATOSPLENOMEGALY (LIVER: 174.7 G, EXPECTED: 130 G; SPLEEN: 14.3 G, EXPECTED: 10 G). B. PETECHIAL HEMORRAGES INVOLVING DIAPHRAGM, THYMUS AND SEROSAL SURFACES. C. HEMATOMAS INVOLVING UMBILICAL AREA (4 x 3 x 1.5 CM) AND ILEOCECAL AREA (2 x 2 x 0.5 CM). D. PERITONEAL EFFUSION, 35 CC, SEROSANGUINOUS FLUID. E. BILATERAL PLEURAL EFFUSIONS, RIGHT: 35 CC, LEFT: 25 CC, SEROSANGUINOUS FLUID. III. CARDIOVASCULAR SYSTEM: A. PATENT DUCTUS ARTERIOSUS. B. PATENT FORAMEN OVALE. C. NO OTHER STRUCTURAL ANOMALIES. IV. NO DYSMORPHIC FEATURES OR CONGENITAL ANOMALIES OF REMAINING MAJOR ORGANS INCLUDING KIDNEYS, LUNGS, GI TRACT. V. ANCILLARY STUDIES: A. LUNG TISSUE AND CSF SENT FOR MICROBIOLOGIC STUDIES: RESULTS PENDING. B. LIVER TISSUE IN GLUTARALDEHYDE FOR POSSIBLE ELECTRON MICROSCOPY STUDY. C. LIVER TISSUE AND MUSCLE SNAP FROZEN FOR POSSIBLE ENZYME ANALYSIS. FINAL CAUSE OF DEATH NEONATAL DEATH ASSOCIATED WITH MULTIORGAN FAILURE, PENDING HISTOLOGIC EXAMINATION AND RESULT OF ANCILLARY STUDIES.

FINAL ANATOMIC DIAGNOSIS I. CLINICAL HISTORY: STILLBORN MALE INFANT OF 28 2/7 WEEKS GESTATIONAL AGE (BIRTH WEIGHT: 720 G, EXPECTED WEIGHT: 864 +/- 247 G), BORN TO A ___YEAR OLD MOTHER, G3P1011 WITH NO SIGNIFICANT MEDICAL HISTORY, WHO PRESENTED WITH DECREASED FETAL MOVEMENT FOR 10 DAYS AND WAS FOUND TO HAVE INTRAUTERINE FETAL DEMISE. CONSENT FOR A FULL AUTOPSY WAS OBTAINED. II. ANTEPARTUM STILLBIRTH: A. NO CONGENITAL ANOMALIES. B. NO DYSMORPHIC FEATURES. C. NO PETECHIAL HEMORRHAGES OVER THYMUS, PERICARDIUM OR PLEURA. D. NO ORGANOMEGALY. III. ANCILLARY STUDIES: A. BLOOD CULTURE: CHRYSEOBACTERIUM MENINGOSEPTICUM. B. LUNG TISSUE CULTURE: STERILE. C. PERICARDIAL TISSUE SENT FOR CYTOGENETICS: NO GROWTH. IV. PLACENTA (S15-10496): CHANGES SECONDARY TO INTRAUTERINE FETAL DEMISE INVOLVING BLOOD VESSELS OF STEM VILLI. V. NEURO EXAMINATION: AUTOLYZED FETAL BRAIN, NO PATHOLOGICAL DIAGNOSIS FINAL ANATOMIC DIAGNOSIS NO ANATOMIC CAUSE OF DEATH FINAL NOTE This is a case of a 28 week and 2 days old male (weight 720 g, expected 1020g ± 340)) stillborn. The mother is a 30y/o g3p1011 with no significant medical history who presented with decreased fetal movement for 10 days. Further examination revealed intrauterine fetal demise. The patient was pronounced dead at __: __am on __/__/____ and consent for a full autopsy was obtained. At autopsy, there were no congenital anomalies noted. There are no dysmorphic features or petechial hemorrhages noted. There was also no organomegaly. Microscopically, there was extensive autolysis, but no major abnormalities were noted. Ancillary studies demonstrated chryseobacterium meningosepticum growth on blood cultures, which is likely a contaminant. The lung culture and cytogenetics tissue had no growth. The anatomic cause of death in this case could not be determined. Chryseobacterium species are normal inhabitants of the soil and water. They are known to exist in water systems and wet surfaces in the hospital environment. It has been known to cause neonatal meningitis in underdeveloped countries due to transmission via the birth canal. It has also been known to cause nosocomial septicemia in immunocompromised and critically ill patients. In this case, it is likely a contaminant from the hospital water system. Unfortunately, there is no anatomic cause of death in this case. The blood culture cannot be relied upon due to the non-sterile nature of how it was obtained. There are no antemortem blood cultures because of the intrauterine demise.

GROSS DESCRIPTION TEMPLATE The patient expired on _/_/_ at __: __am and permission for complete autopsy is given by the WIFE, Mrs. ___ on _/_/_. The autopsy was performed on _/_/_at __: __am. The body is that of a well-developed, well-nourished man weighing approximately __ lb. and measuring __ inches in length, appearing around the recorded age of __years. Liver mortis is slight and unfixed. Rigor mortis is slight and limited to the distal extremities. The hair is not present. Irides are brown. The pupils are equal and round and bilaterally dilated. The sclerae are not jaundiced. The ears and nose are symmetric. The teeth are present. The buccal mucosa is pink. The neck is supple, and trachea is midline. Cervical veins are not distended. The chest is symmetric. The abdomen is soft and obese with multiple thick, white vertical striae. The liver edge and spleen tip are not palpable. There is no pedal edema. The external genitalia are unremarkable. There is a __cm ecchymosis on right inguinal region. The spine appears straight. The extremities are symmetric and well developed. The digits and palmar markings appear unremarkable. There is no clubbing. The skin color is tan with single tattoo and several scars, including tattoo on right arm, and scars on right and left knee (measuring __ cm each), Saphenous vein graft scar on left thigh and leg (measuring __ cm), scar on left forearm (__cm) scar on left wrist (__cm), midline scar on chest (__cm). The following medical paraphernalia are in place: Hospital ID bracelet/tag – right wrist and toe PICC line Intravenous catheter INTERNAL EXAMINATION: The body is opened with a Y-incision. The panniculus adiposus measures 4.6 cm at the umbilicus. There is 80-100ml of clear, yellow-pink serosanguinous peritoneal fluid. The pleural surfaces are glistening and smooth with few lateral adhesions. There is a moderate amount of pleural fluid. The right hemithorax contains 260 ml of blood tinged, serosanguineous fluid; the left contains 180 ml of blood tinged, serosanguineous fluid. Pulmonary arteries are examined with no obvious evidence of pulmonary emboli. The mediastinum is midline. The pericardial sac is open and reveals 50 ml of clear, blood (hemopericardium). CARDIOVASCULAR SYSTEM: The heart is large and weighs 680 grams. The superior and inferior caval veins connect with the right atrium. The tricuspid, pulmonic, mitral, and aortic valves measure 10.5, 6.5, 7, 6 cm respectively. The right and left ventricular chamber are moderately dilated, and its walls average 1.0 cm and 1.5 cm in thickness respectively. There is a moderate amount of epicardial fat. The epicardial surface is smooth with adhesions with pleura. The foramen ovale is non-patent. There are no thrombi in the auricular appendages. The valve leaflets and cusps are mildly thickened. The mitral valve is moderately thickened and calcified. The chordae tendineae are slightly thickened. The endocardial surfaces are smooth. The myocardium is red-brown and shows a recent infarct in the posterolateral wall of left ventricle. The interarterial and interventricular septums are intact. The coronary ostia are patent. The coronary arteries course in the usual fashion and are patent with severe calicifications. They are serially sectioned to reveal plaques or calcifications. No vegetations are appreciated on the valve leaflets or valve cusps. The ascending aorta is dilated and the aorta arches to the left before descending along the left side of the vertebral column. There is a small transmural defect (tear) in the wall of ascending aorta. The major arteries arise from the aorta in the usual configuration. The descending aorta gives off the usual branches. The intimal surface of the aorta is smooth. The aorta is elastic and shows moderate atherosclerosis with a defect (tear) in the ascending aorta. The caval veins and portal vein are patent and thin walled. NECK ORGANS: The larynx is lined by smooth mucosa. There is mild epiglottal edema with tracheal microhemmorhages. PULMONARY SYSTEM: The right lung weighs 630 grams and left lung weighs 560 grams. Both lungs appear moderately congested and slightly anthracotic. Dissection of the pulmonary artery reveals no significant pulmonary thromboembolism. A minor small (0.2cm) suspicious thrombus is identified in a small pulmonary vessel. The embolus/thrombus is retrieved, further confirmation of the true nature of the embolus/thrombus pending microscopic examination. The pulmonary veins are unremarkable. The lungs show no infarcts / lesions. The hilar and tracheal bronchial lymph nodes are not enlarged. There is congestion around the pulmonary vasculature as well as in the dependent portion of the lungs. There is no evidence of aspiration. DIGESTIVE SYSTEM: The esophagus courses in the usual fashion to enter the stomach and its mucosal surface is grey-white and intact with longitudinal folds. No lesions are seen grossly. The stomach contains a small amount of thick brown liquid. Its mucosal surface is intact with tall rugal folds. There are few small brown-pink areas of mucosal erythema. The small intestine is of usual caliber and its walls are pliable. The mucosal surfaces are delicate. The appendix is unremarkable. The colon is of generous caliber with intact mucosa. Multiple diverticuli are seen in ascending, descending and transverse colon, with no congestion / hemorrhage (No gross evidence of diverticulitis) No tumor or polyps are found in the gastrointestinal tract. HEPATOBILIARY SYSTEM: The liver is normal sized and weighs 1470 grams with sharp rounded edges. The capsule is smooth and glistening. The parenchyma is solid red-brown and moderately fatty with a tan to yellow hue. The extrahepatic bile ducts and vessels are patent. A discrete gall bladder is not identified. The pancreas is firm and normal in shape. It is located in its usual position within the duodenal sweep and is surrounded by a moderate amount of fat. On sectioning, the parenchyma is tan-brown and lobulated and shows autolysis. The pancreatic duct is patent to the ampulla of Vater. HEMATOPOEITIC SYSTEM/RETICULOENDOTHELIAL SYSTEM: The spleen is large and weighs 120 grams. It has a smooth, intact capsule with blunted edges. The parenchyma is red-brown and congested. ENDOCRINE SYSTEM: The thyroid gland weighs 34.3 grams and has a symmetrical bi-loped shape. The parenchyma is red-brown and firm. Cut surface show soft red glandular tissue with a single nodule (measuring 0.8 x 0.8cm) identified on the left lobe of thyroid. The right and left adrenal glands weigh 5.1 and 5.4 grams respectively. Both adrenals have uniform yellow-orange cortices separated from the medullary gray by a thin red line. URINARY SYSTEM: The kidneys are located in their usual retroperitoneal position. The right kidney weighs 201.0 grams and left kidney weighs 185 grams. External surface shows multiple scars suggestive of nephrosclerosis. There is a single small, fluid filled cyst on the right kidney surface measuring 0.8 x 0.8 cm. Cut sections of the kidneys reveal red-brown parenchyma with clearly demarcated cortico-medullary junctions and cortical thinning. Bilateral ureters are patent to urinary bladder. The ureteral mucosa is smooth. No stones are seen. The bladder is contracted and does not contain urine. The mucosa is intact. The urethra is patent and unremarkable. REPRODUCTIVE SYSTEM: The prostate is enlarged, firm with lobular gray-white parenchyma and has an evident 0.8 cm x 0.8 cm nodule. The testes are located within the scrotal sac bilaterally and have smooth white capsules. The right and left testes weigh 27.9 grams and 30.9 grams respectively. The parenchyma is tan, and the tubules can be strung with ease. MUSCULOSKELETAL: The cartilage is firm. The bone is hard. The vertebrae, ribs, pelvis, and long bones are intact without gross evidence of fracture. The skeletal muscles are red-brown, firm, and appropriate mass for the patient’s age and sex. The bone marrow of the vertebral column is unremarkable. There is no osteoporosis grossly. CENTRAL NERVOUS SYSTEM: Refer to neuropathological report. SUMMARY OF SECTIONS 1A: RIGHT ATRIUM AND VENTRICLE 1B: INFARCT ON THE POSTERIOR WALL OF LEFT VENTRICLE 1C: INFARCT ON THE POSTERIOR WALL OF LEFT VENTRICLE 1D: LEFT VENTRICLE, NORMAL APPEARING 1E: LEFT ATRIUM 1F: PAPILLARY MUSCLE (FROM LEFT VENTRICLE) 1G: INTERVENTRICULAR SEPTUM 1H: MEMBRANOUS CONDUCTION SYSTEM 1I: LEFT ANTERIOR DESCENDING CORONARY ARTERY, FOLLOWING DECALCIFICATION 1J: CORONARY ARTERY GRAFT LEADING TO LAD (INTERNAL MAMMARY), FOLLOWING DECALCIFICATION 1K: LEFT CIRCUMFLEX ARTERY, FOLLOWING DECALCIFICATION 1L: RIGHT UPPER LOBE OF LUNG 1M: RIGHT MIDDLE LOBE OF LUNG 1N: ECCHYMOTIC AREA FROM RIGHT LUNG AND PLEURA 1O: RIGHT LOWER LOBE OF LUNG 1P: LEFT LOWER LOBE OF LUNG 1Q: LEFT UPPER LOBE OF LUNG 1R: THROMBUS FROM A SMALL PULMONARY VESSEL IN LEFT LUNG 1S: LIVER 1T: LIVER (FATTY CHANGE) 1U: SPLEEN 1V: PANCREAS 1W: RIGHT KIDNEY 1X: LEFT KIDNEY WITH PORTION OF THE CORTICAL SCAR 1Y: CYST FROM LEFT KIDNEY 1Z: RIGHT ADRENAL GLAND 1AA: LEFT ADRENAL GLAND 1BB: RIGHT LOBE OF THYROID 1CC: LEFT LOBE OF THYROID (WITH A NODULAR AREA) 1DD: MUSCLE AND NERVE 1EE: BLADDER 1FF: PROSTATE (WITH A NODULAR AREA) 1GG: DESCENDING AORTA, FOLLOWING DECALCIFICATION 1HH: GASTROESOPHAGEAL JUNCTION 1II: STOMACH 1JJ: APPENDIX 1KK: SMALL INTESTINE (ILEUM) 1LL: ASCENDING COLON 1MM: RIGHT TESTES 1NN: LEFT TESTES 1OO: DECALCIFIED BONE 1PP: DECALCIFIED BONE 1QQ: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (MEDIAL) 1RR: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (MEDIAL) 1SS: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (MEDIAL) 1TT: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (LATERAL) 1UU: RIGHT ATRIUM AROUND THE INFERIOR VENA CAVA (LATERAL) 1VV: RIGHT ATRIUM – ECCHYMOTIC AREA 1WW: RIGHT ATRIUM – ECCHYMOTIC AREA 1XX: RIGHT ATRIUM – ECCHYMOTIC AREA AUTOPSY CHECKLIST ___ Read patient’s chart ___ External Exam ___ Dissection/Gross photos ___ Dictate external exam ___ Rinse organs (next morning) ___ Review with attending ___ Trim case (Bone decal) ___ PAD ___ Dictate Internal exam and Gross description ___ Submit cassettes with decal bone (write cassette range on top of bucket) ___ Check Culture results ___ Slide review/sign out with attending ___ Stains ___ Microscopic description ___ Case Discussion, FAD, final cause of death ___ Submit final report to attending’s worklist MICROSCOPIC DESCRIPTION TEMPLATE HEART: The cardiac myocytes from bilateral ventricles show variation in size and shape, including hypertrophied fibers with enlarged plump nuclei, characteristic of hypertrophy. Interstitial fibrosis is noted bilaterally, and regions of scarring are noted in the interventricular septum. No occlusive atherosclerotic changes are noted in the major coronary arteries with calcifications and recanalization of the occlusion; there is evidence of acute infarction and lymphocytic infiltrates and fibrous adhesions over the epicardium. RESPIRATORY: Sections from the bilateral lungs reveal no emphysematous. Scattered alveolar hemorrhage is noted but with prominent pigment laden macrophages. The sections from lungs show thickened arteries with intimal proliferation, suggestive of pulmonary hypertension. There are no emboli in main pulmonary arteries, but a small pulmonary arteriole shows a small pulmonary thrombo-embolus, showing lines of Zahn. There are no pulmonary infarcts grossly or microscopically. There are scattered foci of interstitial lymphoplasmacytic infiltrates consistent with organizing pneumonia. Diffusely, macrophages laden macrophages are also identified suggestive of congestive cardiomyopathy. HEPATOBILIARY AND PANCREAS: Sections from the liver shows severe autolytic change but no major histopathological abnormality identified. The pancreatic parenchyma displays a normal lobular structure with severe autolysis. GASTROINTESTINAL SYSTEM: The esophagus, and small intestine and the large intestine show normal histology with moderate to severe autolysis. The vessels in the submucosa of the stomach are engorged, consistent with previous episode of bleeding with no histopathological abnormalities. GENITOURINARY SYSTEM: Histologic sections of bilateral kidneys show sclerotic glomeruli and concentric arteriolar thickening suggestive of arteriolar nephrosclerosis. Severe and diffuse autolytic change is noted in the renal tubules. The urinary bladder shows congestion with autolyzed urothelium. Sections from bilateral adnexa are histopathologically unremarkable. RETICULOENDOTHELIAL SYSTEM: The spleen shows normal white and red pulp with moderate congestion. No capsule thickening is identified. MUSCULOSKELETAL: Section of muscle is unremarkable as well as section from peripheral nerve. ENDOCRINE: The thyroid gland shows normal follicular cell and colloid. Adrenal glands show autolytic changes but normal architecture.