ForensicPathologyForum (HISTOPATOLOGÍA FORENSE PRÁCTICA)

21.- POLYCYSTIC KIDNEY AND SUDDEN UNEXPECTED DEATH. PROF.GARFIA.A

2010-02-24T11:48:00.008+01:00

21.-SUDDEN UNEXPECTED DEATH DUE TO BRAIN HAEMORRHAGE IN A LEGAL CASE:HISTOPATHOLOGICAL FINDINGS.
Prof.Garfia.A.

21.-POLYCYSTIC KIDNEY DISEASE AND SUDDEN UNEXPECTED DEATH.
Prof.Garfia.A

CASE REPORT

Bleeding occurs either into brain substance (brain haemorrhage) or into the subarachnoid space (subarachnoid haemorrhage).

The commonest causes of non-traumatic subarachnoid haemorhage (spontaneous haemorrhage) are, in this order:
1) rupture of saccular aneurysm (65%)
2) arteriovenous malformation rupture (5%) and
3) extension of intracerebral haematoma usually into ventricles and then into the subarachnoid space ( 5%)..
About 90% of saccular aneurisms are located in distributions of the internal carotid arteries; the remaining 10% are located on the vertebrobasilar arterial tree. Multiple aneurysms are found in 10-15% of patiens with subarachnoid haemorrhage; these are said to be associated with:

1.- Coarctation of the aorta.

2.- Renal artery stenosis.

3.- Autosomal Dominant Adult Polycystic Kidney Disease ( AD-PCD).

The possible common denominator for the formation of saccular aneurysms is arterial hypertension; however, in AD-PCD there are mutations affecting three genes: PKD1 ( linkage to chromosome 16: 85% of cases); PKD 2 ( 10% of families) and PKD 3. Two of these three genes encode for protein named Policystin I and Policystin II which have an important function in interactions between cells, and between the cells and the extracellular matrix. Abnormal proteins encoded in AD-PCD can play an important role in the origen of saccular aneurysms and in the formation of renal cysts.

In this report it is presented a case of Sudden Unexpected Death due to a Fatal Subarachnoid Haemorrage.
The autopsy demonstrates the existence of a AD-PCD and multiple saccular aneurysms in the vertebro-basilar arterial tree -from one of these originated the fatal haemorrhage- and also a Hipertensive Cardiomyopathy (Heart:770g, with biventricular hypertrophy) unknown for the woman and for the family.

FIG.1.- Gross external appearance of the kidneys showing numerous superficial outstanding cysts on the kidneys surface. Prof.Garfia.A

Fig.2.- Hemisection of one of the two kidneys shows the different size of the cysts and the colloid content inside some of them ( yellow color). Prof. Garfia.A

Fig.3.-Renal cysts occupied by proteinaceos fluid showing striking similarities with thyroid (colloid reabsorption).Note the variability of the cysts size and the flattened epithelium lined it. Prof.Garfia.A

Fig. 4.- Inside some cysts exists papillar grows (or inversion of the tubular pattern: connective tissue inside, tubular epithelium outside. Arrows.).Prof.Garfia.

Fig. 5.- Gross external appearance of heart which shows global hypertrophy (weight:770 g).

PROF.GARFIA.A

Fig.6.- Note the biventricular hypertrophy with severe concentric LV hypertrophy. PROF.GARFIA.A

19.-SUICIDE (PARAQUAT- GRAMOXONE) POISONING: CHROMOPATHOLOGICAL FINDINGS.Prof.Garfia.A

2009-05-12T19:03:00.039+02:00

19.-SUICIDE PARAQUAT POISONING (GRAMOXONE): CHROMOPATHOLOGICAL ESOPHAGUS-STOMACH IMPREGNATION USEFUL FOR THE DIFFERENTIAL DIAGNOSIS IN CASES OF POISONING DUE TO INGESTION OF CHEMICALS SUBSTANCES.

Prof. Garfia.A

A woman 58, years old, was admitted to the Hospital in a cardiorespiratory arrest after she had drank a glass 250 ml containing Gramoxone ( 1,1´-dipiridil-4,54´dipirilon). A Legal Autopsy was carried out which demonstrated the existence of corrosive lesions around the mouth; the esophageal mucosa was partially desquamated and the gastric mucosa showed one perforation through the posterior wall of the stomach.The more characteristic autopsy finding was the intense green color of the mucosa and submucosa of the oesophagus and stomach wall ; in the case of the stomach, from the mucosa until the serosa, all the gastric wall was coloured in green due to the exit of the herbicide into the abdominal cavity through the perforation of the gastric wall.The Gramoxone pH measured from 6-8 and the gastric content pH was 1. The macroscopic lesions can not be attributed, exclusively, to the ingestion of Gramoxone. Inside the glass from which the woman had drank was found hydrochloric acid that she had used to dissolve the Gramoxon.The colicuative necrosis of the esophageal and gastric mucosa was attributed to the action of the alkaline hydrochloric acid.

Fig. 1.- This picture was taken from a bottle of Gramoxone Plus which contains Paraquat and Diquat.Prof.Garfia.A

Fig. 2.- Showing the aspect and the color of the Gramoxone solution. Prof.Garfia.A

Fig. 3.- Esophagus.Macroscopical aspect showing the mucous membrane, necrotic and detached from the submucous layer - as sphacelous necrotic sheets.The submucous layer and the vascular submucous plexus can be seen under the necrotic sheet. Prof.Garfia.A

Fig. 4.- Esophagus. Microscopic section showing the transmural necrosis of the esophagus wall. At the left side is located the mucous membrane; at the right side, the submucous and the muscle layer (coloured in red). Note the difficulty of the tissues to take the dyes-that is very typical when a tisular colicuative necrosis occurs - of the Trichromic Stain. Prof.Garfia.A

Fig. 5.- Esophagus.-Microscopic section of the wall showing the mucous membrane ( on top of the photo), the submucous glands and the severe dilatation of the vessels, due to the caustic effect of the hydrochloric acid. Prof.Garfia. A

Fig. 6.1- Stomach. Macroscopical aspect. Note the intense green color of the gastric serosa due to the pass of the Gramoxone through the perforation located in the posterior wall of the stomach.Prof.Garfia.A

Fig.6.2.- The gastric mucosa was focally necrotic and coloured in emerald green. In those areas were the mucous membrane layer was absent we can see the submucous vascular net, due to the severe congestion and dilatation of the small submucous vessels. Prof.Garfia.A

Fig. 7.-Stomach. Showing the microvascular pattern of the submucous layer. The caustic effect of the hydrochloric acid on the microvessels produced vasodilatation and congestion which, together with the coloured effect of the Gramoxone, showed the microvascular pattern of the submucous layer. Normally that is only possible using silver impregnation technics ( see: Garfia.A.-Glomus tissue in the vicinity of the human carotid sinus region.Journal of Anatomy. 132:1-12.1980). Prof.Garfia.A

18.- LARYNX AS TARGET ORGAN OF ANAPHYLACTIC REACTION IN AN ASTHMATIC PATIENT.Prof.Garfia.A

2009-04-18T08:29:00.024+02:00

18.-FATAL OBSTRUCTIVE EDEMA OF THE ARITENOEPIGLOTTIC FOLDS FOLLOWING AN ANAPHYLACTIC REACTION IN A ASMATHIC PATIENT.

PROF.GARFIA.A

Fatal upper airway obstruction can occurs in children and in adults people.In young children is most commonly caused by inhaled foreing bodies, particularly due to food or toy parts.Much less frequently fatal compromise of the superior airway occurs due to an congenital malformation such as a lingual thyrod at the base of the tongue (see:http://www.forensic-histopathology-garfiaa.blogspot.com), from the same author), or a lingual thyroglossal duct cyst. Acquired lesions may also result in fatal airway narrowing and often involve an infectious etiology such as acute epiglottitis, or acute inflamation of a lingual tonsil.Many of these cases occurs in infancy and very early chilhood, although food aspiration, so called "cafe coronary death" may occur at any age. A special chapter in adults it is referred to deaths due to Anaphylactic Reactions after insect bites - wasp,hornets and bees- or deaths following drug administration sometimes difficult to diagnostised due to some drugs are drugs normally utilized againts the anaphylactic process, such as metilprednisolone or other corticoids which utilize "carboximethylcellulose" as disolvent.

CASE REPORT

A finnish man, 58 years old, with pathological antecedents of alergical illnes, arterial hypertension and bronchial asthma presented an undiagnosed clinical picture of pain in the right half of the face, accompanied by important facial and lingual edema.Soon after, the patient went to the Hospital Emergency Service and, after 3 hours, transferred to Intensive Care Unit, where he suffered cardiorespiratory arrest and die.

The medicament treatment guide was the following:

At Home

Urbason....60mg.i.v.

Amoxicillin..875 mg/12 hours.

Antihistamines...(unknown).

Few hours later the clinical picture suffers progresive worsening and the patient go to the Urgency Hospital Service.At the Hospital, the patient presented severe lingual and laringeal edema.The Medical team administrated:

Actocortin...300mg+

Urbason......40 mg, dissolved in a 100ml ampoule of physiological serum. After that, the patient presented a convulsive picture and cardiorespiratory arrest and was sended to the Critic Unit.The orotracheal intubation with a Sheridan tube number 6, was not possible.The patient received the following medication:

Adrenalin: two bolus of 20mg.

Atropine......3mg.

Salbutamol. 3mg

The patient went to cardiovascular arrest and die after 70 min. of cardiopulmonary resuscitation.

Photo nº 1.-Macroscopical aspect of the larynx, posterior aspect. To note the severe obstructive edema (arrows) of the arytenoepiglottic folds (stars) and the erasure of the cuneiform and corniculate tubercles of the right side due to the brutal suffocating edema, typical of the larynx anaphylactic response. The differential dignosis must be made with the infectious acute fatal epiglottitis, where the affectation of the inflamation affects, more specifically, to the epiglottical structures. Prof.Garfia.A

PHOTO Nº 2. To show the microscopical aspect of the arytenoepiglottic folds.Note that the inflamation is due to the edema with scanty cellular componente inside it. This is the second characteristic of the anaphylactic affectation of the larinx (anaphylactic target organ in asthmatic people). Ep=epithelium. Ed= edema.Prof.Garfia.A

PHOTO Nº 3.- To show the scanty cellular component (arrows) inside the edema in the anaphylactic reaction. Cells are, principally, leucocytes eosinophiles and plasma cells (the third characteristic of the laringeal anaphilactic reaction). Masson Trichrome-stain.Prof.Garfia.A

17.-FAMILIAL MYOCARDIAL INFARCT.PROF. GARFIA. A

2009-04-02T12:00:00.026+02:00

17.-SUDDEN CARDIAC DEATH DUE TO SEVERE CORONARY ATHEROSCLEROSIS IN A YOUNG MAN, 26 YEARS OLD.
PROF. GARFIA.A

A 26 year old patient who died as a consequence of myocardial infarction in the presence of witnesses.Two weeks earlier he had visited his family doctor for pain in his shoulder and left arm, which was diagnosed as muscular strain for which the patient was recommended to place his arm in a sling.The pathological study showed the existence of a myocardial infarct in the interventricular septum and the scar was two weeks old.The left circumflex coronary and the anterior descending arteries, presented severe atheromatous stenosis, of more than 90%. Among the points of interest in the family history, the existence of two episodes of myocardial infarction with hospitalization in the Intensive Care Unit of the victim's elder brother, aged 32 years, due to a myocardial infarct and the death of a first cousin 28 years old - also due to myocardial infarction - were significant.Given the youth of the deceased and his family history, the convenience of carrying out a lipid study was suggested to the family, in view of the suspicion of possible familial hiperlipidaemia.The results of the autopsy, together with the familiy history, the biochemical and the lipid study carried out pointed to the existence of a Combined Primary Familial Hiperlipidaemia. Other possibility to explain the severe atheromatous lesions found in this case would be the existence of an abnormal elevation of Lipoprotein (a) ( > 0.3 g/L), - considered by numerous authors an independent risk factor to have conditioned the apparition of a severe atherosclerotic coronariopathy and sudden cardiac death in young people- was unfortunatelly not determined in this case.

.

Photo 1.- 26 year old patient.The left anterior descending coronary artery showing severe lumen narrowing due to coronary atherosclerosis (arrow). The red line inside the artery show the residual arterial lumen. Prof.Garfia.A

Photo 2.-Microscopical aspect of the same artery showing the severe narrowing of the lumen ( more of 90%) due to the existence of a fibroatheromatous plaque with fibrin deposition (arrows), probably dependent of the organization of a previous trombus (L=lumen). Prof.Garfia.A

Photo 3.- Microscopical section of the left circumflex coronary artery showing a severe narrowing of the lumen due to the existence of a typical fibrous cap atheroma which contains a necrotic core containing cholesterol clefts, foam cells and fibrous tissue.Prof.Garfia.A

Photo 4.- Right coronary artery. It shows intimal hyperplasia -with fibrous tissue and foam cells- but the reduction of the arterial lumen (L) is not so severe than in the others coronaries arteries. Focal preatheromatous lesion.Prof.Garfia.A

Photo nº.-5.- Showing an intramyocardial arteriole which presents a thicker muscular wall -and penetration of connective tissue from the adventitia- for the age of the patient. Prof.Garfia.A

Photo nº.6.- This section of the heart shows the localization of the myocardial infarct (arrows) in the interventricular septum.Prof.Garfia.A

Photo nº. 7.- The mycroscopical study of this area demonstrated the existence of a myocardial infarct -aproximatelly two weeks old- due to the presence of granulation tissue plenty of macrophages cells with cellular debris and neocollagen fibers formation. (IAM= myocardial infarct). Prof.Garfia.A

16.-INTRACARDIAC DEVICE EVALUATION AT AUTOPSY.II PROSTHETIC VALVES.Prof.GARFIA.A AND REPETTO.F

2009-03-16T12:47:00.003+01:00

15.-CARDIAC ATRIAL TUMOR VERSUS ORGANIZED THROMBUS AND SUDDEN UNEXPECTED DEATH.Prof..Garfia.A

2009-03-11T19:09:00.023+01:00

15.-ATRIAL TUMOR AND SUDDEN UNEXPECTED DEATH.

Prof. Garfia.A

A fithty year old man in good health, suffered an acute heart failure secondary to obstruction of blood flow, and was pronounced dead, at his home.During a legal autopsy a heart weighing 540 g was found, which showed biventricular hypertrophy ( RV: 0.8 cm; LV 2.0 cm ); the left heart was moderately dilated. At the left atrium was detected a polipoid tumor, 6 cm diameter in its biggest dimension, which was attached, on a broad base, to the atrial septum (fossa ovalis). The tumor had a villous appearance and presented gelatinous areas intercalated with haemorrhagic areas.The left atrium was almost filled by the tumor which extended down into the mitral valve orifice. The histological appearance of the tumor was very variable in different areas examinated.The bulk of the tumor is made up of a myxoid stroma and embedded in the stroma were the myxoma cells which shows polygonal, spindle or stellate-shaped.The term "lepidic" (scale-like) has been applied to these cells due to their polygonal aspect. In some areas can be seen spaces lined by endothelial cells to which the myxoma cells are loosely attached. Inside the macroscopic haemorrhagic areas the tumor shows numerous vascular spaces of telangiectasis aspect. Also, other elements found in the matrix include haemorrhage foci, old and more recent, located besides the telangiectasis spaces.The differential diagnosis must be made with low-grade sarcomas, so named "myxoid imitators".Sometimes, the distinction between organized thrombus and myxoma, is very difficult.Virtually any cardiac tumor may cause sudden death through a variety of mechanismus including rhythm disturbances, embolization and acute heart failure secondary to obstruction of blood flow.Cardiac myxomas are- generally- tumors found in adults, and present as sudden death in aproximatelly 5% of cases due to embolization to the coronary arteries, acute obstruction of the mitral valve, or also, cerebral embolization

Atrial myxomas are the most common primary benign tumour, show a slight female predominance and are, generally, located in in the left atrium. Generally, myxomas are solitary tumors, however, a familial myxoma syndrome has been described: it is called NAME, (acronyms of N: blue naevi; A: Atrial myxoma; M: mucocutaneous myxoma; E: ephelides) or LAMB ( L= lentigines; A= atrial myxoma; M=mucocutaneous myxomas; B blue naevi). In the familial syndrome the tumours can be multiple and located also in a ventricle.

Photo nº 1 .-To show the macroscopical aspect of the tumor in the left atrium. Prof.Garfia.A

Photo nº 2.- Gross Pathology:tumoral surface.The tumoral surface - mamelonne- shows different aspects and colours, from the red-wine, and haemorrhagic aspect, until pearly-white colour. Prof.Garfia.A

Photo nº 3.- Atrial myxoma. Shows the hystology of the components of myxoma: free-floating spindle and stellate cells -sometimes syncytial-; myxoid ground substance, and a surface layer. Prof.Garfia.A

Photo nº 4.- Shows a very characteristic appearance of myxoma cells arranged in a cuff around a small central space.Prof.Garfia.A

Photo .- 5.- Some cells show nuclei similar to the Anitschkow cells found in the rheumatic carditis (spindle -shaped cells showing ovoid open vesicular nuclei and condensation of the chromatin toward the nuclear membrane - caterpillar cells). They are considered as a variety of mesenchymall cell readily induced in the connective tissue of the heart, in young individuals, by a wide range of insults. Prof.Garfia.A

14.-TURPENTINE POISONING:REPORT OF A FATAL CASE.Prof.Garfia.A

2009-03-10T14:12:00.024+01:00

14.-Fatal Poisoning due to Suicidal Ingestion of Turpentine Solution. Autopsy and Histopathological Findings.

Prof.Garfia.A

A -40 year old- woman was admitted to the Intensive Care Unit with coma and apnea. There was insufficient information about the manner and the speed of coma onset, as she had been found by her relatives, in her room, where she was laying unconcious, on the floor.The woman was under treatment with antidepresive and ansyolitics drugs prescribed by a psychiatrist doctor.The patient was treated with hemoperfusion and was pronounced dead due to multiorganic failure, two hours later. A legal autopsy was done.Turpentine ingestion was suspected from the beginning of the autopsy due to the pine odor of the corpse.The relatives said that they found a bottle of Turpentine beside the patient's bed.The more important findings during the autopsy were relative to the gastrointestinal system, specially at the oesophagus and the stomach; both organs show dark blood on the mucosa surface and the stomach was dilated and contained 120 ml of a dark bloody liquid.The organ show several perforations and can be seen gastric contents in the peritoneum with necrosis of the spleen capsule. Samples of gastric fluid and blood contain cyclic terpenos, normal components of pine oil.Turpentine is a colorless thin transparent oily liquid with a strong specific odor (pine odor; violet odor), insoluble in water but soluble in numerous organic solvents. It is used to dissolve oil-based paints, varnish and grease stains. During acute poisoning with Turpentine, the more important clinical manifestations occur in the gastrointestinal system -nausea, vomiting and diarrhea- and in the Nervous System, as coma or stupor. The acute toxic oral dose has been estimated in excess of 2 mL/kg. Systemix toxicity, when it appears, ocurs two or three hours after the exposure. The main metabolite of monoterpenes ( the main constituents in turpentine solutions), named bornylacetate, has a peak excretion in urine the 5th and 6th post-exposure day.Hemoperfusion eliminates turpentine constituents effectively from the blood and only should be applied at an early stage of intoxication before accumulation of the toxins in tissues be established.Inmediate and continous gastric lavage is the most effective therapy.

Foto A.- Show a very important gastric dilation due to the colliquative necrosis and gastromalacia of the organ.Prof.Garfia.A

Foto B.- Exposed gastric mucosa, after the opening, showing the colliquative necrosis and the gastric hemorrhage. Prof.Garfia.A

13.-AUTOPSY EVALUATION OF INTRACARDIAC DEVICES. I.- PACEMAKERS. Prof.GARFIA.A

2009-03-08T19:11:00.034+01:00

13.-INTRACARDIAC DEVICES EVALUATION: A FACE UP TO THE AUTOPSY PATHOLOGIST.

I.- PACEMAKERS.

Prof.GARFIA.A

Implantable devices for the management of the cardiac illness is increasing; for this reason a pathologist can found an intracardiac device during his professional life. Several types of devices can be found implanted in the heart, such as: cardioverter-defibrillators, pacemakers, prosthetic heart valves, occluder devices, stents, etc. The material used for the differents types of devices can be inorganic - polyfluorocarbons, cobalt and titanium, chromium alloys, ceramics- or biologic ( fascia lata, dura, bovine and porcine pericardium,etc).

Pathologist's Role at Autopsy.-

At the autopsy, the pathologist must examine for degenerative changes in presence of prosthetic valves, and also for ring abcesses, perivalvar leaks, or strut fractures in Björk-Shiley prostheses with occluder escape -which are rare complications of mechanical valves. Degenerative changes with infection and perforation are not unfrequent in bioprosthetic valves. In cases of suspect pacemaker malfunction must be investigated the pulse generator and the leads -it is said: test of the battery, pulse width, sensing function and integrity of leads. Some iatrogenic complications include entrapment of the pacingwire in the tricuspid valve, neointima formation around the lead adjacent to the tricuspide valve and tip,and fibrous thickening at the tip encasing the lead within endocardial tissue ( see fotos 5-6-7). In opinion of some authors, these changes are not necessarily associated with the age of the pacemaker and the inclusion of the leads inside the right ventricular wall explains the reason for the problems to extracting pacemakers from living patients.

Foto nº 1.- To show the leads components of a dual chamber pacemaker "in situ", after the opening of the right atrium. Prof.Garfia.A

Foto nº 2.-Sagital section through the right heart in order to follow the course of the pacemaker. AD=right atrium. VD= right ventricle. VDPA= rihgt ventricle anterior wall. VT= mitral valve. Arrows showing insertion points of the leads in the right heart. Prof.Garfia.A

Foto nº 3.- Detail to show the organic -fibrin and platelets- sheath created around the metallic lead which lies in the atrium in this dual chamber pacemaker. Prof. Garfia.A

Foto nº4.-Detail of the friable sheath around the metallic envelope of the atrial lead. Prof.Garfia.A

Foto nº 5.- To demonstrates the ventricular lead, which has incited a fibrotic reaction (arrow) in the right ventricular wall (neointima formation). This fibrous reaction may make extraction of the device difficult - must be necessary open heart surgery to do it. Prof. Garfia.A

Foto nº 6.-Examination with microscopical polarized light to demonstrate the structure of the fibrous thickening sheath (neointima=mfib) around the tip of the lead. (ele= lead). Prof.Garfia.A

Foto nº 7.- The fibrous neointima (mfib), surrounding the lead, contains some giant cells (cg) in the proximity to the lead (ele = lead). Prof.Garfia.A

12.-SUDDEN DEATH AT THE EMERGENCY SERVICE OF AN ANXIOUS PATIENT.Prof.Garfia.A

2009-02-28T12:05:00.036+01:00

12.-SUDDEN UNEXPECTED DEATH AT THE HOSPITAL EMERGENCY SERVICE OF AN WOMAN TREATED FOR ANXIETY NEUROSIS.Prof.Garfia.A

Patients who suffer serious psychiatric problems, and those others whose symptoms are half way between purely emotional disorders and those dependent on somatization of psychological conflicts, make up a group of patients for whom diagnosis requires special attention and effort. The first form a group at high risk of unexpected death from illnesses so common that it is really surprising that they are not diagnosed and treated in time. The second are faced with the difficulty at diagnosis of differentiating between the truly emotional and the somatic, with the secondary danger of obviating the real somatic cause of some clinical state, with symptoms easily labelled as psychological. At times reality asserts itself drastically, and is legally conflictive for the doctor or the hospital team. We present a case of unexpected death, which took place at the Medical Emergency Service, of a patient diagnosed with anxiety neurosis. The forensic autopsy discovered the existence of a pheochromocytoma of the left adrenal gland .

Cases of sudden unexpected death associated with the tumor pathology occur seldom.Generally, tumors can causes "truly" sudden death when they provocated serious circulatories problems, such as brain haemorrhages -leucemies- or fatal haemoptisis; massive pulmonary embolization and/or tumoral pulmonary embolization ( liver and digestive system tumors); or massive carcinomatosis ( primary tumors found in the breast, digestive system, pancreas and genital organs).This tumor, the pheochromocytoma, can produce serious cardiovascular pathology, inclusive sudden death, due to the excessive producction of chemical messengers which can produce an overstimulation in the Cardiovascular System, originating a toxic nor-epinephrin myocarditis - due to a direct toxic effect on the myocardiocites; between these messengers are the Adrenalin and Nor-adrenalin and the peptide named adrenomedulin.

CASE REPORT

In this report it is presented a case of a woman, 50 years old, who was attended at the Hospital Emergency Service at 3.00 hours in the morning. She had a clinical syntomatology consisted of: abdominal pain, dyspnea, and vomiting with blood- tinged froth. The arterial pression was 12/6 and the ECG presented sinusal rythm 120 x. The woman go to the observation room and presented a little later, progressive dyspnea and the followings parameters: Ph 7.21; PCO2 33; PO2 50; HCO3- 13; and O2 saturation 77%. Posteriorly,the woman presented two episodes of cardiac arrest, being necessary aplication of avanced RCP. The patient was transported to the Unit Care and connected to assisted ventilation; in that moment, the arterial pression was 60/0, the ECG shows a sinusal rythms to 130x', a Glasgow of 3 and arreactive mydriasis. Two hours later the patient was pronounced dead. A clinical diagnosis of cardiogenic shock and pulmonary edema of cardiogenic origin was emitted.The family solicited a legal autopsy.The macroscopic examination demonstrated the existence of a tumor located in the left renal fossa of 8x5x4,5 cm of maximal diameters (Foto nº 1). Both kidneys were normal.The lungs showed pulmonary edema, and the rest of the organs were normal. Microscopically the epicardial and intramural arterioles in the heart showed hypertensive changes ( see Foto nº 2) and also the renal arterioles.The tumor was rounded for a capsule of conective tissue but we can found some tumoral cells penetrating the capsule.Tumor cells were polygonals and they had an ample cytoplasm, brownish, occupied by acidophile granulations.The nuclei were rounded and sometimes giant and pleomorphic. Inside the tumor we found some ganglionar cells and also nests of the glomerulous cells of the adrenal gland ( see Fotos 4-5). The heart shows very abundant focus of myocardiocites presenting contraction band necrosis which do not show a coronary distribution pattern dependence. A diagnostic of epinephrine myocarditis (focal myocarditis) was emitted and was considered the cause of death.

FIG. 1 .-Macroscopical aspect of the pheochromocytoma (feo), located in the left renal fossa. Left kidney (ri).Prof. Garfia.A

FIG.2.- Epicardial (above) and intramural (below), arterioles showing hypertensive changes.Prof.Garfia.A

FIG.-3 Multifocal contracction band necrosis of myocardiocytes (arrows) expression of a ephinefrine myocarditis.Prof.Garfia.A

FIG.4 .- Showing nest of tumoral cells with poligonal form. Tumoral capsule (cap).Prof.Garfia.A

Fig.5.- Nest of tumoral and ganglionar cells inside the tumor. Arrows showing rests of glomerulous cells of the adrenal gland. Prof.Garfia.A

REFERENCES

1. Garfia A, Borondo J.- Muerte súbita en Patología Forense. Rev Esp Med Legal.Enero-Junio 1989; pp. 31-43.

2. Garfia A.- Glomus tissue in the vicinity of the human carotid sinus. Journal of Anatomy 130: 1-12 (1980).

3.- Garfia A.- En Böck, P.- The Paraganglia. Handbuch der mikroskopischen Anatomie. Band 6. Blutgefäß- und Lymphgefäßapparat. 8 Teil.Springer-Verlag. Berlin1982. pp.89.

4.- Garfia A.- Muerte Súbita o Retardada asociada a la Patología del Compartimento Lateral del cuello: el papel fisiopatológico de los Barorreceptores del Seno Carotídeo y de los Quimiorreceprores del Glomus Caroticum. Cuad Med For 16-17. 1999. 85-153

5.-Garfia et al.-Vascular lesions in the intestinal ischaemia induced by Cocaine-Alcohol Abuse:Report of a Fatal Case due to Overdose.Journal of Forensic Science.Vol 35.nº 3.1990

6. Henle J.- Allgemeine Anatomie. Leipzig 1841.

7. Henle J.- Über die Gewebe der Nebenniere und Hypophyse. Z rat Med 24, 143-152 (1865).

8. Rosai J.- Ackerman´s Surgical Pathology. 7ª Ed. Ed Mosby C. Washington D.C. 1989.

9. Cotran R, Kumar V, Robbins S.- Pathological Basis of Disease. Interamericana. 1995.

10. Silver MD, Gotlieb AI, Schoen FJ.- Cardiovascular Pathology. Churchill Livingstone.N.Y. 2001.

11. Karch SB .- The Pathology of Drug Abuse. 3ª Ed. CRC Press. 2002. pp. 104.

12. Szakacs, J and Cannon, A.- L-Norepinephrine myocarditis. Am J Clin Pathol. 30, pp. 425-434.

13. Van Vliet, Burchell HB, Titus JL.- Focal myocarditis associated with pheochromocytoma. N Engl J Med 274:1102-1105. 1966.

14. Jessurun CR, Adam K, Moisek J Jr, Wilansky S.- Pheochromocytoma-induced myocardial infarction in pregnancy. Tex Heart Inst J 20:120-124;1993.

15. Morris K, McDevitt B.- Pheochromocytoma presenting as a case of mesenteric vascular occlusion. Ir Med J 78:356-358.1985.

16. Gulliford MC, Hawkins CP, Murphy RP.- Spontaneous dissection of the carotid artery and pheochromocytoma. Br J HospMed 35: 416-420, 1986.

17. DeSouza TG, Berlad L, Shaphiro K et al.,- Pheochromocytoma and multiple intracerebral aneurysms. J Pediatr 108: 947-950. 1986.

SUDDEN DEATH IN ADOLESCENT.PROF.GARFIA.A

2009-02-27T18:58:00.016+01:00

11.-SUDDEN AND UNEXPECTED DEATH IN AN ADOLESCENT:INTESTINAL DUPLICATION. Prof.GARFIA.A

CASE REPORT

It is presented a case of sudden unexpected death, in a 19 year-old adolescent, who in the hours prior to his death presented a clinical picture of dizziness, nausea and vomiting which was treated at the First-Aid Centre with analgesics and antispasmodics. After a few hours the patient was again taken to the Medical Centre by his relatives, by then unconscious. In spite of resuscitation measures the patient presented cardio-respiratory arrest and sudden death. During the autopsy the existence of a mesenteric tumor was discovered in the distal ileum. The corpse gave off a peculiar smell which reminded the Prosector of the typical smell of some organophosphorous pesticides. The following diagnoses for the cause of death were put forward in the autopsy report:

1.- Septic shock due to intestinal abscess. 2.-Mortal poisoning by pesticides. 3.-Sudden death of cardiac origin. The chemical investigation resulted negative. The histopathologic study did not show cardiac lesions which could justify the death. The investigation of the intestinal tumor showed that it was a cystic intestinal duplication, with a slight chronic inflamation of the intestinal wall duplication. Perforations, haemorrhage, ischaemic or vascular intestinal lesions which could have justified sudden unexpected death -with digestive causes- were not seen.

The Cause and Manner of Death were considered undetermined.

FIG. 1.- To show the macroscopical aspect of the cystic intestinal duplication. The cystic wall was similar to the intestinal wall and we found -inside the cyst- a sebaous-gelatinous material brownish. Prof.Garfia.A

FIG.2 .-To show the intestinal normal wall (above) and the cystic intestinal duplication wall (down).Prof. Garfia.A

LI.- Intestinal normal lumen.

LDU.- Lumen of the cystic duplication.

M.- Mucosae.

S.-Submucosae.

MI.-Internal Muscularis.

ME.- External Muscularis which is shared between the normal intestinal wall and the cystic wall duplication.

FIG.3.- The cystic mucosae( m) appeared constituted by several layers of macrophagical cells (arrows) and cellular necrotic debris on the luminal surface. Prof.Garfia.A

FIG. 4.- Shows the external cystic wall. Mi= internal muscularis.ME=external muscularis. SP= peritoneal serous. Note the slight linfocitary infiltration in the muscularis wall and focally in the peritoneal serous. Prof.Garfia.A

FATAL AORTIC STAB WOUND.Prof.Garfia.A

2009-02-24T21:50:00.030+01:00

10.-FATAL AORTIC STAB WOUND.

Prof.Garfia.A

CASE REPORT A man 27 years old, who was a drug abuse addict, was stabbed -on the street during an arguement with a man part of a group- with a self-made weapon consisted of a wooden bar, 1.5 mtrs long which was supported, at one end with a pointed knife and the other end with a sharp hammer edge. The homicide was arrested and the weapon found at his house. The autopsy demonstrate an incise wound in the right side of the thorax which penetrated the right lung and the right heart ventricle. The pericardiac sac shows a haematoma, at tension, and at the aortic wall a dissecting haematoma. We received the heart with the dissection made following the haemodinamic outflow with exposition and opening of the aortic valve. Macroscopically, the heart -260 g - showed a stab wound in the anterior wall of the right ventricle, near the atrioventricular groove, which penetrated into the aorta where could be seen an entrance wound, and an exit wound located at the posterior wall of the aorta ( see. fig.2); it measured 1 cm long and orientated parallel to the aortic cusps of the aortic valve which penetrated through the aortic wall (trans-aortic stab wound); the exit wound in the posterior side of the aortic wall was plugged with the dissecting haematome.

Foto 1,2,3.- Weapon used for the murdered, self-made, with a hammer in one extreme and a knife in the other. The bar was 1.5 mtrs long.Prof.GARFIA.A

Foto 4.-Stab aortic wound. Note the anterior face of the exit wound in the posterior aortic wall. The exit wound is plugged due to the dissecting haematome.(asterisc). Prof.GARFIA.A

9.- ADENITIS TUBERCULOSAS PERIAÓRTICAS EN SUJETO DROGADICTO.PROF.GARFIA.A

2009-02-24T18:43:00.025+01:00

9.-ADENOMEGALIAS PERIAÓRTICAS EN SUJETO DROGADICTO VIH +.
Prof. Garfia.A

CASE REPORT

Varón de 30 años, adicto a la heroína, VIH +, que en el momento del fallecimiento se encontraba en tratamiento con metadona. En la necropsia se demostraron adenomegalias, de más de tres centímetros y de consistencia aumentada, que afectaban a las cadenas ganglionares preaórticas, aórtico-laterales y retroaórticas, del grupo linfático lumbar. Macroscópicamente, la aorta abdominal y segmentos de la vena cava inferior, aparecían rodeados por un manguito perivascular, segmentario, adenomegálico, que constituía una auténtica envoltura tubular periaórtica. El estudio microscópico puso de manifiesto la existencia de una linfadenitis granulomatosa caseificante; alrededor de los extensos focos de necrosis existía un infiltrado inflamatorio constituído por linfocitos y células plasmáticas, así como por células gigantes multinucleadas, escasas. La tinción, con la técnica de Ziehl-Neelsen demostró la existencia de abundantes bacilos localizados en el citoplasma de células de características macrofágicas. En los sujetos vivos, la punción aspirativa ganglionar, mediante aguja fina, ha permitido definir en el Sida un patrón denominado linfadenitis necrosante, que se caracteriza, en el examen citológico del material obtenido por punción, por la presencia de grandes cantidades de material necrótico -sobre una base granular difusa de color rosa a púrpura- con la tinción de May-Grünwald-Giemsa. El hallazgo de una linfadenitis necrosante es suficiente, en clínica, para iniciar un tratamiento con tuberculostáticos en los pacientes infectados por el VIH. Si no fuese posible la realización de la punción aspirativa, o de la biopsia, el diagnóstico diferencial con otras causas de adenomegalias, tales como: toxoplasmosis, sífilis, leishmaniasis, síndrome de Epstein-Barr, etc. se deberá realizar mediante estudio serológico excluyente, por el PPD (Mantoux) y por la búsqueda del bacilo de Koch en otros órganos (pulmón, por la asociación tan frecuente de la tuberculosis ganglionar con la pulmonar) mediante estudio en aspirado gástrico, esputo, hemocultivo y orina. En los enfermos de SIDA el PPD suele ser negativo a partir del estadio IV, independientemente de que exista tuberculosis activa. Por otro lado, la falta de cooperación entre los linfocitos T y B (secundaria a la afectación de los linfocitos CD4 por el VIH) impide obtener respuestas IgM de fase aguda en las seroaglutinaciones, por lo que debe tenerse en cuenta que una serología negativa no excluye una enfermedad, en el contexto del SIDA. El Mycobacterium avium y el Mycobacterium intracellulare son dos micobacterias muy relacionadas entre sí, que se han agrupado y se conocen con el nombre común de Mycobacterium avium complex (MAC o MAI). El MAI es la micobacteria más frecuentemente encontrada en los enfermos de SIDA y la causa más frecuente de infección bacteriana diseminada dentro de este grupo. La forma diseminada de linfadenitis por MAI suele ocurrir en los estadios terminales de esta enfermedad. El MAI es una micobacteria que se encuentra en el suelo, en el agua y en las plantas y es transportada por los pájaros y los animales de las granjas. La infección humana por MAI es poco frecuente y se consideran no patógenos para el hombre u ocasionalmente oportunistas. En los pacientes inmunodeprimidos, no SIDA dependientes, la infección por MAI puede originar una respuesta granulomatosa caseificante aunque esta respuesta no es frecuente en los enfermos de SIDA, tal como sucede en este caso. El hallazgo morfológico diagnóstico es la presencia de bacilos teñidos de rojo con la técnica de Ziehl-Neelsen localizados en el interior del citoplasma de células macrofágicas. Los bacilos se tiñen , también, con la técnica de Giemsa, con el PAS, con la plata-metenamina, y con la tinción de Brown-Hoops (Hum Pathol 18: 709-714,1987. y Am J Clin Pathol 85: 233-235, 1986).

FOTOS A Y B.- CORRESPONDEN A CORTES TRANSVERSALES (A) Y LONGITUDINALES (B) DE LA AORTA ABDOMINAL.NÓTESE EL MANGUITO PERIAÓRTICO CONSTITUIDO POR LAS NUMEROSAS ADENOMEGALIAS (GL), DE LAS CADENAS PERIAÓRTICAS LUMBARES. Prof.GARFIA.A

FOTO C.- Corte microscópico que muestra la adenitis granulomatosa necrotizante. Las adenomegalias aparecen constituidas por folículos linfoides hiperplásicos que presentan necrosis central (flechas), rodeada por una corona linfocitaria, mal conformada,en el seno de la cual se detectan células gigantes multinucleadas, de Langhans. Tricrómico 150x. Prof.GARFIA.A

FOTO D.- Detalle de dos células gigantes multinucleadas. Tricrómico 400x. Prof.Garfia.A

FOTO E.- Bacilos intracelulares demostrados con la técnica de Ziehl, en las áreas de necrosis, en forma de bastoncillos de color rojo.(flechas).630x.Prof.Garfia.A

8.-SUDDEN DEATH DUE TO SUBARACHNOID HAEMORRHAGE IN A WOMAN 49 YEARS OLD.Prof.GARFIA.A

2009-02-20T18:18:00.038+01:00

8.-POLYCYSTIC KIDNEY DISEASE AND SUDDEN DEATH.

PROF.GARFIA.A

CASE REPORT

Bleeding occurs either into brain substance (brain haemorrhage) or into the subarachnoid space (subarachnoid haemorrhage).The commonest causes of non-traumatic subarachnoid haemorhage (spontaneous haemorrhage) are, in this order:1)rupture of saccular aneurysm (65%) 2) arteriovenous malformation rupture (5%) and 3) extension of intracerebral haematoma usually into ventricles and then into the subarachnoid space ( 5%). About 90% of saccular aneurisms are located in distributions of the internal carotid arteries; the remaining 10% are located on the vertebrobasilar arterial tree.Multiple aneurysms are found in 10-15% of patiens with subarachnoid haemorrhage; these are said to be associated with:

1.- Coarctation of the aorta.

2.- Renal artery stenosis.

3.- Autosomal Dominant Adult Polycystic Kidney Disease ( AD-PCD).

In this report it is presented a case of sudden death due to a fatal subarachnoid haemorrage.
The autopsy demonstrates the existence of a AD-PCD and multiple saccular aneurysms in the vertebro-basilar arterial tree -from one of these originated the fatal haemorrhage- and also a Hipertensive Cardiomyopathy (Heart:770g, with biventricular hypertrophy) unknown for the woman and for the family.

FIG.1.- Gross external appearance of the kidneys showing numerous superficial outstanding cysts on the kidneys surface. Prof.Garfia.A

FIG.2.-Hemisection of one of the two kidneys shows the different size of the cysts and the colloid content inside some of them ( yellow color as fat aspect).Prof.Garfia.A

FIG. 3 Inside some cysts exists papillar grows (or inversion of the tubular pattern: connective tissue inside, tubular epithelium outside.Arrows.).Prof.Garfia.A

FIG.4.-Renal cysts occupied by proteinaceos fluid showing striking similarities with thyroids colloid. Note the variability of the cysts size and the flattened epithelium lined it. Prof.Garfia.A

FIG.5.-.-Gross external appearance of heart which shows global hypertrophy (weight:770g).

Prof. Garfia.A

FIG.6.-Note the biventricular hypertrophy with severe concentric LV hypertrophy. Prof.Garfia.A

7.-TOXIC EPIDERMAL NECROLYSIS FATAL RELATED TO PHENITOYN ADMINISTRATION.PROF.GARFIA.A

2009-02-17T19:24:00.024+01:00

7.-TOXIC EPIDERMAL NECROLYSIS FATAL AND PHENITOYN.
PROF.GARFIA.A

CASE REPORT

Untowards reactions to drugs are an important medical problem, sometimes followed by a fatal outcome. Although drugs reactions may involve any organ system, cutaneous eruptions drug-induced may result from a drug administered by any route, which reactions can be identified more frequently than other toxics drug-depending effects which occurs in other organs, such as liver and kidney, because their visibility. Toxic epidermal necrolysis (TEN) or Lyell's Syndrome, is one of the most dramatic, the most severe, and one of most often studied cutaneous drug reactions. TEN is characterized by extensive detachment of the epidermis nuder-going full-thickness necrosis. The drugs more frequently implicated are: anticonvulsivants (phenitoyn, phenobarbital, carbamazepine);antibiotics (ampicillin), sulfonamides and nonsteroids antiinflamatory agents (phenylobutazone, oxyphenbutazone, isoxicam,piroxicam and allopurinol).

We report here a fatal case of TEN related to the anticonvulsivant drug phenitoyn, which was prescribed a man, 74 years old, one month before in order to treat a temporal epilepsy, secondary to a stroke (residual epilepsy).

FIG.1.-A.-To show a diffuse macular and papular erythematous eruption that rapidly becomes confluent and widespread followed by flaccid fluid filled bullae (B) which rapidly ulcerate, leaving painful raw erosions similar to scalding. Mild pressure on erythematous areas may produce (C) detachment of the epidermis (positive Nikolsky sign) and aspect of wet cloth of the epidermis. As result, there may be large areas of exposed dermis resembling a burn (C). Prof.GARFIA.A

FIG. 2 .- The histopathological features of early lesions of toxic epidermal necrolysis are those of an extreme degree of epidermal keratinocyte necrosis (2A), associated with subepidermal blistering (2B, arrows), as a consecuence of basal cell hydropic degeneration.
In more mature lesion, there is complete separation of the epidermis (2C) and the roof of the subepidermal bulla is, usually, necrotic.
2C.-Showing necrotic epidermis completely separated from underlying dermis and to note the paucity of dermal inflamatory infiltrate.Prof.GARFIA.A

6.-SUDDEN DEATH AND RENAL ONCOCYTOMA.Prof.Garfia.A

2009-02-11T22:32:00.037+01:00

6.-ONCOCYTOMA RENAL AND SUDDEN UNEXPECTED DEATH.

PROF.GARFIA.A

CASE REPORT

The case is described of a 57 year-old male who died suddenly in the field where he worked. The body was found several hours later and showed erosion and bruising on the right temple, coinciding with the zone of impact on falling to the ground. From the medical history the family pointed out the existence of a stroke, cardiopathy and non-insulin dependent diabetes.
At autopsy the heart (520 g) shows left concentric ventricular hypertrophy.It was found the existence of a spherical renal tumor about 6 cm in diameter, and orange color on cutting; the centre of the tumor was a cystic cavity lined with whitish fibrous-like tissue.
The probable causal relationships between the existence of the tumor, the hypertensive heart disease and stroke, suffered by the man, and his sudden death is discussed.

Oncocytoma and chromophobe cell carcinoma are two well recognised histological entities in the current classification of renal tumors. Both entities are closely related and arise in the distal portion of the neprhon or in the collector tubules. From a forensic point of view, it is important to point at the incidental autopsy finding of this tumor and, until we know, the classical triad of palpable mass, flank pain or hematuria was absent in this case.

I think that Sudden Death presentation was consecuence of the Hypertensive Heart Disease and the oncocytoma, unfortunatly, an incidental autopsy finding.

Fig.1.- Gross examination shows a well circumscribed tumor, with encapsulated appearance (arrows), uniforme yellow color and with a central stellate cystic scar (C) which shows striking similarities with a pathological renal pelvis. Is it a kidney (collecting tubules and pelvis) inside the Kidney? Prof.Garfia.A

Fig. 2.- Detail to show the seudocapsule (arrows), and the central stellate cystic scar (C). Prof.Garfia.A

Fig.3.-Microsscopical aspect of the seudocapsule (arrows).Prof.Garfia.A

Fig.4.-To show the microscopic tubular pattern inside the tumor (arrow: transversal tubular section from a good differentiated tubule) and differents longitudinal tubular sections (T), where we can see how some tubules are originating from others through a gemmation process (T, at the right side). Haematoxilin-eosin-floxine. Prof.Garfia.A

Fig. 5.-Reticulin stain to demonstrate basal membranes which show a microscopic tubular pattern delimiting renal tubules (T). Prof.Garfia.A

Fig.6.-In others microscopical fields some structures show striking similarities with primitive glomeruli and contain a tuff of mesangial matrix (M) containing primitive capillaries (at the rihgt figure, just over the letter M. Prof.Garfia.A

5.-TOXIC HAEMORRHAGIC PERIPHERAL NEUROPATHY FOLLOWING POISONING BY RODENTICIDES AND SOLVENTS.Prof. GARFIA.A

2009-02-11T19:14:00.026+01:00

5.-TOXIC HAEMORRHAGIC PERIPHERAL NEUROPATHY.

PROF.GARFIA.A

CASE REPORT

It is described a case of mortal poisoning by ingestion of the Rodenticide Brodifacoum, a superwarfarin anticoagulant, together with other drugs, among which were non steroid anti-inflammantory drugs and a domestic organic solvent. The individual died in the Intensive Care Unit, with acute respiratory insufficiency, followed by hepatic and renal failure. At autopsy perineural rounded haemorrhagic lesions were seen, wich affected several tissues, among which were mesenteric fat, the epicardium and the perikidney fat. Microscopy study revealed the existence of a typical acute haemorrhagic lesion, located around the epicardial vegetative nerves and those found in the splanchnic beds. The reason why the peripheral vegetative nerves constitute the target of the toxic effects was attributed to the combined action of the solvents with the superwarfarine drug on the Peripheral Nervous System. It is known that organic solvents produce an acute neuronal lesion, consisting in tumefaction of the axon and the neuronal soma, which leads to the alteration of the system of transport ( neurotubules) along the axon. We believe that -from a physiological point of view - the reactive vascular congestion of the vasa-nervorum - produced as a consecuence of the acute neuronal lesion induced by the solvents, together with the state of hipocoagulability of the blood, due to the ingestion of superwarfarin Brodifacoum, and potentiated by the anticoagulant action on the non steroid anti-inflamatory drugs, make up the intimate mechanism which could explain this characteristic Acute Toxic Haemorrhagic Neuropathy of the peripheral nerves of the Neurovegetative Nervous System. We do not know if the mixed peripheral nerves were affected by this lesion due to absence of samples for a more definitive study.Although most cases of brodifacoum poisoning in humans are non-fatal, this compound, alone, can be deadly because of its very long half-life. In Forensic Pathology we must suspect superwarfarin rodenticides poisoning when confronted with cases of unexplained bleeding. Anticoagulant poisoning can mimic leukemia or infectious diseases such as bacterial sepsis, leptospirosis or rickettsioses; a death scene investigation may provide clues that a person has ingested these substances.

Fig.1-Showing an Acute Toxic Haemorrhagic Neuropathy affecting a nerve (N) located at the peripancreatic fat. Arrows delimiting the perineurium. Note the aspect " in diana" of the haemorrhage in the plane of this thin slice cut (H= haemorrhagic perineural "sheath" when we thought in three dimensions). PROF.Garfia.A

4.-MASSIVE PULMONARY EMBOLIZATION WITH CEREBRAL TISSUE AND LAMELLAR BONE SPICULES DUE TO GUNSHOT WOUND TO THE HEAD.Prof.Garfia.A;Palomo.J.L.

2009-02-07T14:05:00.028+01:00

FIG.-7.-Scheme showing the direction of the bullet in the head: from back to front and from occipital (left) to temporal lobe (right). Prof. Garfia.A

FIG.-6.- Embolization with cerebral tissue (ETJC) inside a pulmonary artery (AP). Prof.Garfia.A

FIG.5.-Details to show the brain tissue as a component of the embolus ( arrows: piramidal cortical brain neurons). Klüver-Barrera. Prof.Garfia.A

FIG.- 3B.- Show the same artery examinated with polarized light (hu lam): the bone spicule is formed of lamellar adult bone. Masson. Prof.Garfia.A

FIG.3A.-Embolization of bone spicules (arrows) to the lung. Pulmonary artery (stars). Bone spicule (hue- arrows). Masson trichrome stain. Prof.Garfia.A

Fig. 2.-Liver.Right lobe. Superior face. Penetrating entrance gunshot wound showing stellate aspect. Bullet caliber 22. Prof.Garfia.A

FIG. 1.- Superior pole of the right kidney. Note the deep niche leaved for the projectil during his trajectory from front to back (arrows). Prof.Garfia.A

Venous and arterial embolism of endogenous tissue components and foreign material must be considered, in forensic pathology, as markers of vital reactions. Pulmonary embolization of cerebral tissue following severe head trauma or due to gunshot wound to the head is uncommonly reported at autopsy. Embolism of bone marrow to the lung is a quite frequent finding after trauma but transport and deposition of solid bone is rarely seen.

CASE REPORT
Prof.Garfia.A

We report one case of pulmonary embolization with cortical cerebral tissue and with fragments of adult lamellar bone due to gunshot wound to the head in a 32-year-old woman. Brain tissue embolization may have a significant impact on the premortem clinical management of the head trauma patient due to that brain tissue is well known to cause plasma coagulation, shock, and consumptive coagulopathy upon direct contact with the blood stream. These haematologic events have the potential to play a significant role in the morbidity and mortality of head trauma patients. From a statistical and public health perspective, cerebral tissue pulmonary emboli should be sought in all autopsied cases of death due to head injury.

2009-01-25T08:00:00.002+01:00

2009-01-21T18:48:00.163+01:00

3.- AIR EMBOLISM AND DEATHS SCUBA DIVING IN SPAIN.
PROF. GARFIA.A

Deaths associated with scuba diving have become more numerous in Spain due to the increase in popularity of this recreational sport; many people believe that diving sport is not a dangerous sport and anyone can practice it, irrespective of their present state of health or other influences that can affect the physiological conditions under the water (alcohol, drugs,etc.) To the best of my knowledge, it is not necessary to obtain a Medical Certificate to practice this sport in anyone of the numerous schools on the Spanish coast who have introduced this popular sport. When death occurs during the practice of this sport or professional diving, using scuba equipment, though criminality is rarely a factor, in Spain, a forensic autopsy to determine the cause and the manner of the death, in the event of a request for compensation, which may lead to a civil case. Decompression of a diver ascending to the surface is, by far, the most common accident as a source of injury and death. In the professional diving field there is an increased activity associated with the offshore oil industry -the most dangerous type of commercial employment in other countries such as Britain, Venezuela,USA, etc. Most of these companies make sure for insurance purposes that their divers are fit and have Medical Certificates on a yearly or six month basis since they are paid very high salaries. Hazards of scuba diving, are: drowning and those secondary to barotrauma - pressure changes associated with descent and ascent- which describes the mechanical damage from gas released into the tissues. The bends (caisson disease; decompression sickness), air embolism, acute pulmonary emphysema, pneumothorax and related conditions are some of the more common examples; carbon monoxide intoxication occurs rarely, Paul-Bert intoxication ( acute neurotoxicity due to oxygen hyperbaric 100% concentrated), Lorrain-Smith effect (cronic pneumotoxicity),hypoxy and caustications due to soda lime are complications due to inhalation of hyperbaric oxygen with scuba closed circuit. The bends (caisson disease, decompression sickness) is due to a rapid decompression and occurs if the diver remains for a prolonged period of time at depths at which rapid changes of ambient pression cause the formation of bubbles in his blood and tissues. Rapid decompression may result in embolism of gas bubbles in two different ways: 1) air that expands but cannot escape the lung may damage the lung tissue (barotrauma) and be forced into the pulmonary vessels. The diagnosis of a venous air embolism, regardless of its cause, relies largely on the macroscopic examination findings. The venous air embolism can be diagnosed much more reliably in the course of an early autopsy, in order to find the presence of air bubbles, or frothy blood, inside the right heart, arteria pulmonalis, afferent cardiac large veins and coronary veins, than by microscopic examination. It is said: the diagnosis of venous air embolism is macroscopic although, microscopically, the presence of air bubbles in pulmonary arteries can be recognized by their outlines within the blood colums. 2) gas dissolved in the blood will be released in the form of small bubbles. In this case (caisson disease-decompression sickness), the presence of a lot of bubbles in the systemic circulation (arterial air embolism) has far greater consecuences than their embolization to the pulmonary vessels. Evidence of arterial air embolism is not easy to demonstrate and relies, largely, on the microscopical findings. After a short survival time of a few hours, the air disappears out of the vascular areas and organs affected, by resorption. However, sometimes it is possible to find the embolized air in the microscopic sections of several organs, such as brain, lungs, spleen, liver and kidneys. In this work I show the microscopical findings, with special reference to air-embolism, found in five cases of death during the practice of sport scuba diving, in Spain. The differential diagnostic must include the formation of postmortem gas emphysema (putrefaction cadaveric phase), in different organs -specially, liver, lung and heart- where the putrefaction air bubbles can show striking similarities with the air bubbles embolisms. For these reasons the autopsy must be carried out as soon as possible, preferably, within 24 hours.

CASES REPORTS

CASE Nº 1.-

Prof.Garfia.A

A man 30 years old, proffessional diver and teacher in a school of scuba diving, made an immersion, by night, after a great intake of alcohol. He was accompanied by a pupil who talked to him to persuade him not to make the immersion, due to his high intake of alcohol. The man was under the water for one hour. After this time the pupil rescued him, cadaver. Autopsy findings were typical of drowning and gas bubbles were found in the right ventricle and the liver, squeezing under the water during the autopsy delivered small air bubbles. Microscopically, air bubbles were found in the gastric wall -muscularis mucosae-, in the brain and in the kidneys. The stomach shows a acute haemorrhagic gastritis which was attribuited to the high alcohol intake ( one bottle of gin), in the observation of the pupil witness.

CASE Nº 2.-

Prof.Garfia.A

A man, 26 years old, was found dead in the sea when he was practicing sport scuba diving in the South Spanish coast. He was under the water, approximately, 30 minutes and to 10-15 meters of profundity. The macroscopical autopsy demonstrate heavy aedematous lungs but few macroscopical signs of drowning death. The more important microscopical findings were found in the cerebellum cortical layer: multiple cortical microhaemorrhages. The lungs and the heart show air embolism ( see figs. 1 and 2 ) and pulmonary oedema and emphysema. The rest of the organs showed inespecific congestion.

CASE Nº 3

Prof.Garfia.A

Woman, 40 years old, doctor, with antecedents of hypertension and diabetes.Obesity (90 kg). She was a pupil of a scuba diving course. Two months before, during the practice of scuba diving she had an accidente very similar to the actual. In that moment the woman was under the water to 10-20 meters of profundity and suddenly she was unconscious. Members of the team brought her to the surface and she was admitted to the nearest Hospital. She was in the Intensive Care Unit for 2 days and was treated with hyperbaric oxygen (50%). In the Unit, she presented dysnea and chest pain. A diagnosis of demi-drowning and Hypoxemic Respiratory Failure was emitted. Actually, the situation was similar; a member of the team related that the woman gives the alarm signal and she was transported to the surface in 20 seconds ( the profundity was, in that moment, of 20 meters). Once in the boat she was unconscious and on arrival at the Hospital she was pronounced dead. Autopsy demonstrates intense pulmonary congestion and very important edema with blood-tinged froth, in the nose, mouth, and distal respiratory passages and also interstitial pulmonary emphysema and pneumothorax. During the microscopical investigation, air bubbles were found in the following organs: brain, meningeal vessels, liver, kidney and spleen. Lungs show acute pulmonary emphysema. The more important finding was located in the heart ( 460 gr), with hypertensive cardiomyopathy and a severe narrowing arteriolopathy affecting the papilar muscles of the left ventricle. Also in the liver, hepatocytes showed glycogen vacuolization of nuclei- a specific marker of diabetes mellitus.

CASE Nº 4

Prof.Garfia.A

A man, 22 years old;. no pathologic antecedents. He belonged to a diver team who were doing immersion in groups. During the last immersion one member of the team saw one diver went out of the group and notice that he had open arms and legs, which appeared to be seperated from his body. Once member of the team came over to chek his condition and found him to be unconscious; this diver checked was unconscious and he had not the mouthpiece located in position normal; the diver intend to put him the self-mouthpiece but due to the unconscious state of him he can not do it. that the joung man and his mouth piece was not located in the normal position, and he was unable to replace the selfmouth piece due to his unconscieous state. Together with his partner they managed to re-surface him in 15 minutes. The man was dead when he arrived on the surface. The partner to decided to transported him to the surface, in 15 seconds. The computer-clock marked a deep of 101 meters and the time neccesary to go the surface was of 15 minutes. The coast police commented that it is not allowed diving under 60 meters.

Autopsy demonstrated multiple air bubbles inside the vascular compartment - heart, coronary venous vessels, and meningeal vessels- and also multiple haemorrhagic petechials in over the pleural surface. Microscopical investigation (see Figs.4) demonstrated air bubbles inside the vascular compartment of cerebellum, liver, lung and myocardium. The rest of the organs show unspecific congestion.

CASE nº 5

Prof. Garfia.A

A professional choral fisherman, age 30 years, was working at the Spanish coast in the proximity of Cádiz. The Police was called from a ship, who later arrived at the Port with a corpse of a young man. The Forensic Medical external examination of the dead body shows an extensive blood tinged froth extended all over the face - mouth and proximal respiratory passages.Although this finding is also seen in pulmonary edema from any cause, such as drug overdose, severe head injuries and congestive heart failure. The assistant personnel on the ship told the Police that the man was 40 minutes under the water at a deep of 75 meters. After that time the personnel of the ship went to look for him, and finally found him dead. The autopsy demonstrated haemorrhage in the middle ears, bilaterally; lungs showed intense pulmonary congestion and multifocal edema, and the stomach contained a lot of air due to the fact that it was largely distended. Microscopical investigation demonstrated the presence of air bubbels inside the vascular net of the brain, lungs and kidneys (see Figs. Case 5).

Case nº 5. Air embolism. Scuba diving.Death. Cerebellum. Note the air bubbles inside the cortical layer and also inside the meningeal vessels. Prof.Garfia.A

Case nº 5. Air embolism.Scuba diving.Death. Cerebellum. Air bubbles inside the cortical cerebellum vessels. Prof.Garfia.A

Case nº 5. Heart. Air embolism. Scuba diving. Death. Prof.Garfia.A

Case nº 5. Heart.Air embolism.Scuba diving.Death. Note the different morphological aspects of air bubbles. Prof.Garfia.A

CASE Nº4. Lung. Scuba diving death.Elastic pulmonary artery contains two air bubbles. Prof.Garfia.A

CASE Nº4.-Heart.Scuba diving death. Air embolism. Note the compression of the myocardiocytes. Prof.Garfia.A

CASE Nº4.-Liver.Hematoxilin-Eosin.Sinusoids air embolism.Scuba diving. Death. Prof.Garfia.A

CASE Nº 4- Scuba diving death. Liver.Air embolism in the sinusoids (german sausage aspect).
Prof. Garfia.A

CASE nº4.-Scuba diving death. Liver.Reticuline stain.Numerous air bubbles in a portal space. Prof.Garfia.A

Case nº 3.- Liver. Central vein. Scuba diving air embolism. Note how the air bubble made a pressure tunnel inside the continuous blood colum. Prof. Garfia.A

Case nº 3.- Liver. Central vein distended by air bubble. Prof.Garfia.A

Case nº 3.- Liver. Air embolism.The portal vein branch appears distended by the air bubble.
Prof. Garfia.A

Case nº 3.- Brain. Air bubbles in the white matter. Prof. Garfia.A

Case nº 2.- Detail to show the compression of the myocardiocites around the gas bubble (star).
Prof. Garfia.A

Case nº 2.- Air bubbles in the heart capillaries (stars). Prof.Garfia.A

Case nº 1.- Lung. Acute pulmonary emphysema, pneumothorax and air embolism may be considered, togheter, as they are all different stages of the same phenomenon.The mechanism responsible for the development of these conditions, single or in combination, is excessive pressure in the lungs. Prof.Garfia.A

Case nº 1.- Fig.1.- Air embolism and death during sport scuba diving. Gastric wall. Air bubbles inside vessels of the muscularis mucosae. Prof. Garfia.A

Case nº 1.- Fig.2.- Gastric wall showing multiple haemorragic foci in the mucosa which was attributed to the high alcohol intake (toxic haemorrhagic gastritis). Prof.Garfia.A

Case nº 1.- Kidney. Shows air bubbles in the capillaries located in the medulla. Prof.Garfia.A

Case nº 1.-Kidney. To show an air buble inside a renal arteriole. Note how the pression of the air buble dilate the vascular lumen of the arteriole. Prof.Garfia.A

2.-FORENSIC PATHOLOGY PRACTICAL FOR PATHOLOGISTS, JURISTS AND LEGAL MEDICINE SPECIALISTS.PROF.GARFIA.A

2009-01-10T14:08:00.021+01:00

http://www.forensicpathologyforum.blogspot.com/

http://www.forensic-histopathology-garfiaa.blogspot.com/

FORENSIC PATHOLOGY FORUM

Prof.Garfia.A

1.-PULMONARY EMBOLISM OF CARDIAC TISSUE DUE TO GUNSHOT WOUND TO THE THORAX.Prof.Garfia.A

2009-01-08T18:56:00.027+01:00

1.-MARKERS OF VITAL REACTIONS IN FORENSIC HISTOPATHOLOGY:PULMONARY EMBOLISM OF CARDIAC TISSUE DUE TO GUNSHOT WOUND TO THE THORAX.

PROF. GARFIA.A

FIG. 1.-PULMONARY EMBOLISM OC CARDIAC TISSUE DUE TO GUNSHOT WOUND TO THE THORAX. PROF.GARFIA.A

FIG. 2.- PULMONARY EMBOLISM OC CARDIAC TISSUE DUE TO GUNSHOT WOUND TO THE THORAX. ARROWS SHOW THE CHARACTERISTICALLY CENTRALLY PLACED NUCLEI OF THE CARDIAC MYOCYTES. PROF.GARFIA.A

Venous and arterial embolisms of endogenous tissue components and also foreing material must be considered, in Forensic Pathology, as marker of vital reactions.On the other hand, must be borne in mind that, during the putrefactive cadaveric phase can be produced embolization of clusters of hepatic cells due to the putrefactive gases which can propelled it from the liver or other compact organs into the veins of the pulmonary circulation. Lung capillaries functions as a sieve in the blood circulation and various material can be trapped there. Bone marrow embolism is very frequently founded after trauma, reanimation procedures and bone surgery, -specially after methalic prothesis implants, due to the great destruction of bone tissue during the surgical procedure. Pulmonary embolism of bone spicules is a very rare event and sometimes ocurrs after trauma ocurring in a septic bone lesion, or accompanying to the cerebral tissue embolism to the lungs due to gunshot wound to the head. However, embolism of cardiac muscle cells to the lungs is vey rare type of embolism of organ fragments. It has been previously described following the operation on an atrial septum defect in a child.

Case Report

A little girl 16 year old was admitted to Hospital because she had received a close range gunshot wound from a revolver 44 Magnum. She was pronounced death at the arrival in the Hospital. On postmortem examination was found one entrance wound gunshot located at the right shoulder and an exit wound gunshot located between the 9th and 10th left ribs, through the intercostal space. Internal examination demonstrated a rounded hole surrounded by hemorrhagic infiltration, 1.5 cm diameter, which connect with the interventricular septum and perforating it, obliquely, in the way to the posterior face of the left ventricle; here, can be found an exit wound, rounded, affecting left ventricle, posterior interventricular septum and a small part of the wall of the right ventricle. Microscopic lungs examination demonstrate the presence of a lot of emboli of cardiac tissue inside the alveolar pulmonary capillaries.