Morphological findings after tracheotomy and laryngeal intubation (author's transl)]

4 fatal cases after tracheotomy and 35 cases after endotracheal anaesthesia were examined taking pathomorphological aspects into consideration. In long-period intubation mucous membrane necroses occurred as of the 4th day. After 6 days' intubation skeletizations of the tracheal rings were established in each case. Infections of the decubial ulcers and errosion haemorrhages from the necrotically altered tracheal wall were frequent complications. Faulty intubation of the oesophagus and the right bronchus, aspirations and reflex-related circulatory failure during intubation as well as hypoxic damage as a result of the windpipe opening being impaired are discussed from the morphological point of view.     

Asphyxia by tracheobronchial thrombus

Asphyxia secondary to airway obstruction has numerous underlying causes, both acute and chronic. Causes of chronic airway obstruction, such as neoplasms and tracheal scarring, are often clinically apparent well prior to asphyxia. Causes of acute airway obstruction may not be as obvious to clinicians or investigators. These include infections, anaphylactic reactions, status asthmaticus, inhalational injuries, and aspirations, which may result in acute obstruction and sudden death.We report the deaths of 2 individuals, a 43-year-old female and a 78-year-old female, both with adenocarcinoma. The 43-year-old was hospitalized with a stage III, poorly differentiated infiltrating ductal carcinoma of the breast metastatic to the lymph nodes. She was intubated to treat poor respiratory function and acidosis. A bronchoalveolar lavage was consistent with alveolar hemorrhage; no organisms were identified. Blood and "clot" were in her endotracheal tube, so the endotracheal tube was replaced. She became comatose and life support was withdrawn. At autopsy, a large red-gray thrombus obstructed the trachea and extended into the right bronchus. Microscopically, the entire clot was composed of fibrin, red blood cells, and some mucus. Findings of acute respiratory distress syndrome with hyaline membranes were identified. The cause of death was listed as acute respiratory distress syndrome with tracheobronchial thrombus. Experiencing a decline in mental status, the 78-year-old had metastatic adenocarcinoma of unknown primary. She developed sudden respiratory distress and an airway obstruction was discovered. After failure to relieve the obstruction, she decompensated and died. At autopsy, a large, red-gray thrombus obstructed the distal trachea and both bronchi. Microscopically, the thrombus was composed of fibrin, platelets, and red blood cells. The cause of death was asphyxia secondary to airway obstruction by thrombus. We present these 2 unusual cases of asphyxia and review of the literature focusing on asphyxia and the etiology of airway thrombi.     

Potentially lethal complications of tracheostomy: autopsy considerations

Tracheostomy is widely used to facilitate respiration by protecting the airways. It may be performed to relieve upper airway obstruction from congenital stenoses or from acquired conditions such as foreign body impaction, swelling from neck trauma or anaphylaxis, benign or malignant tumors, and infection. Tracheostomy may also be performed in individuals with respiratory impairment who require suctioning for accumulated mucoid secretions and in those with obstructive sleep apnea. Review of autopsy files and the literature was undertaken to demonstrate the range of lethal circumstances that may involve tracheostomy. Unexpected death may result from incorrect positioning of an endotracheal tube with failure of oxygenation, tracheal perforation with pneumothorax, mucus plugging, accidental extubation, and hemorrhage from tracheovascular fistulas. Lethal tracheovascular fistulas usually involve the innominate artery and result from mural perforation by the tip of a tracheostomy tube, mural necrosis from a high-pressure cuff, prolonged intubation, radiotherapy, and low tracheal incisions. Increased movement of tubes in patients with impaired consciousness and excessive head movements may also increase the chances of hemorrhage, as may infiltrating tumors. Given the wide range of potential fatal mechanisms that may be found in such cases, careful autopsy evaluation and dissection will be required to demonstrate the exact nature and site of the lethal lesion in individuals who underwent tracheostomy and die unexpectedly.     

Endobronchial/Tracheal Metastasis and Sudden Death

Endobronchial and endotracheal metastases are rare lesions that may cause acute occlusion of major airways. A case is reported of a 62‐year‐old man with history of renal cell carcinoma and hemoptysis who died after having suddenly become short of breath with cyanosis. At autopsy, recurrent renal cell carcinoma was identified with metastases to the lungs, pulmonary hilar lymph nodes, and brain. In addition, a solitary papillomatous metastasis arising from the mucosa of the carina was obstructing both the main bronchi and distal trachea. Death was due to acute airway obstruction by a metastatic deposit at the bifurcation of the trachea in a case of disseminated renal cell carcinoma. This case demonstrates an extremely rare cause of sudden death that may complicate disseminated malignancy.     

Artifactual injuries of the larynx produced by resuscitative intubation

Over a period of 9 months we examined a series of 50 deaths due to natural and unnatural causes in which there had been endotracheal intubation and chest compression during resuscitation at the scene or in the emergency department shortly before death. In 37 of 50 cases (74%) there were airway injuries directly resulting from the intubation procedure which we documented using a standardized protocol and photography. Specific airway injuries, ranging from petechiae to contusions, included oral injury (28%), posterior pharyngeal injury (16%), epiglottic injury (22%), piriform recess injury (12%), laryngeal and tracheal mucosa injury (64%), strap muscle hemorrhage (14%), and cutaneous injury of the neck (4%). In addition, we recorded the presence of facial (6%) and conjunctival petechiae (21%) and attributed these changes to resuscitative chest compression. No cases had associated fractures of the hyoid or thyroid cartilage. Based on our findings, we conclude that resuscitative intubation can cause artifactual injury that may mimic inflicted injuries caused by neck compression, including strangulation and neck holds.     

Fatal splenic rupture following Heimlich maneuver: case report and literature review

The most effective resuscitative procedure in choking by foreign bodies is the Heimlich maneuver, described for the first time by Henry Heimlich (1974) and recognized by the US Surgeon General (1985) as the "only method that should be used for the treatment of choking from foreign body airway obstruction." If performed correctly, this lifesaving maneuver is associated with rare complications, of which the most frequent are rib fractures and gastric or esophagus perforations. Other rare traumatic injuries such as pneumomediastinum, aortic valve cusp rupture, diaphragmatic herniation, jejunum perforation, hepatic rupture, or mesenteric laceration have been described.However, we are unaware of previous reports of splenic rupture after Heimlich maneuver. We present an interesting case of fatal hemoperitoneum due to a hilar laceration of the spleen following a correctly performed Heimlich maneuver.     

Respiratory,Circulatory, and Neurological Responses to Hanging: A Review of Animal Models

Abstract: The pathophysiology of hanging is still poorly understood. This article presents a review of eight animal models: four models of isolated occlusion of the vessels of the neck (group 1), one model of combined tracheal and vessel occlusion (group 2), and three models of true animal hanging (group 3). Occlusion of the airway passages in group 2 did not accelerate respiratory arrest compared to group 1. Cessation of cerebral blood flow, rather than airway obstruction, seems to be the main cause of respiratory decline. In general, muscular movements ceased after 1–3.5 min and early generalized tonic‐clonic convulsions were described. Complete circulatory collapse seems to occur between 4 and 8.5 min. These observations from animal models of hanging are compared with the data collected from filmed human hangings. Avenues to improve animal models are discussed.     

Determining the state of the deceased during cardiopulmonary resuscitation from tissue distribution patterns of intubation-related lidocaine

The objective of this study was to determine whether the concentrations of lidocaine, used for endotracheal intubation, in body fluids and tissues reflect the state of the circulation of the deceased during cardiopulmonary resuscitation. The tissue distribution of lidocaine was investigated in seven individuals (Cases 1-7) who underwent medical treatment with endotracheal intubation using Xylocaine jelly (a 2% lidocaine hydrochloride preparation), before being pronounced dead. Six patients (Cases 1-6) had cardiopulmonary arrest on arrival at hospital. In Cases 1-4, there was no restoration of heartbeat during cardiopulmonary resuscitation. However, systemic distribution of intubation-related lidocaine was observed and the kidney-to-liver ratios of lidocaine were less than 1. In Cases 5 and 6, the heartbeat resumed temporarily with cardiac massage, and a kidney-to-liver lidocaine ratio greater than 1 was observed. In Case 7, where the patient was comatose upon admission to hospital, the kidney-to-liver ratio of lidocaine was also greater than 1. These phenomena were substantiated in animal experiments. Our results indicate that the absorption of tracheal lidocaine during the artificial circulation resulting from cardiopulmonary resuscitation results in a kidney to liver ratio of less than 1, whereas absorption during natural circulation gives a ratio greater than 1. The kidney-to-liver ratio of intubation-related lidocaine may give useful information on the state of a patient during cardiopulmonary resuscitation.     

Ultrastructural differences of fibrin coagulation before and after cardiovascular arrest

The reconstruction of killing offences often requires the differentiation between vital and postmortal blood traces at the sites of action and finding. Earlier investigations seemed to imply the possibility of such a differentiation depending on the different clot structure. We therefore examined clots prior and after 10 minutes of complete occlusion of the upper extremity morphologically and morphometrically with the REM. The morphologic comparison of these clots revealed narrow, round shaped fibrin fiber networks for clots of native blood, whereas clots after occlusion showed linear, rarely connected long fibrin fibers. The morphometry of the fibrin free spaces revealed a significant enlargement of the single fibrin free spaces as well as of the total fibrin free space after occlusion. For capillary blood a significant decrease in fiber diameter was observed after occlusion. The examination of clinical clotting parameters revealed alterations of thrombocyte aggregation for the collagen induction, a slightly reduced thrombocyte retention and slightly steeper flanks in the thromboelastogram after occlusion. The reason for these changes was interpreted as lack of high energetic phosphates in the retraction process as the clotting cascade itself requires a very high amount of these phosphates. Use of these results in the forensic practice will have to take factors as temperature, drying out, surface-structure and many others into account.     

Azygos vein laceration due to blunt trauma

The azygos vein ascends along the thoracic spine through the mediastinum and drains into the superior vena cava at the level of the fourth thoracic vertebra. Fracture-dislocation of the mid-thoracic spine, as a result of blunt thoracic trauma, can tear the azygos vein. Four such fatal cases (three motor vehicle accidents and one fall) were studied, only one of which was recognized prior to death. The vein can also be torn, in the absence of skeletal injuries, by horizontal acceleration/deceleration forces. The pathologist must consider azygos vein laceration as a possible cause of either hemothorax or hemomediastinum or both in a victim of a blunt chest trauma, if that individual had persistent hypotension during the few hours before death and no identifiable source of hemorrhage can be found postmortem in sites such as the heart, great vessels, lung, and chest wall. A fracture-dislocation of the thoracic spine may not necessarily be present. Azygos vein laceration seems to be an uncommon cause of hemothorax and hemomediastinum; however, this injury is probably more frequent than is implied by the few cases described in the medical literature.     

Sudden infant death: lingual thyroglossal duct cyst versus environmental factors

An 8-month-old female baby was found collapsed in the prone position 30 min after being positioned under soft-bedding. She was taken to the emergency room with cardiopulmonary arrest. Her heartbeat was recovered after resuscitation and continued for 20 h under artificial respiration, at which point the child died. At autopsy, the child showed no significant pathological abnormalities apart from a thyroglossal duct cyst of 2.0 cm diameter, therefore, it seemed that the cyst, which was close to the epiglottis, had caused asphyxia through airways occlusion. However, the child had shown no respiratory problems before death, and the risk of airway occlusion as a result of lingual cysts is more likely in a supine rather than a prone position. A small amount of evidence suggested that the child died as a result of suffocation from being covered by soft-bedding, which could have caused fatal asphyxia; it is also possible that a hypoxic state induced by airway obstruction might have been enhanced by being covered with bedding. It seemed reasonable to assume that death was caused by a combination of the lingual thyroglossal duct cysts and asphyxia caused by being covered in bedding, though the main factor appeared to be the large cyst.     

Tissue distribution of lidocaine in critical care patients after intubation

We investigated tissue distribution of lidocaine in 33 patients after endotracheal intubation with Xylocaine jelly that contains 2% lidocaine hydrochloride. Blood levels of monoethylglycinexylidide (MEGX), an active metabolite of lidocaine, were also determined. Five patients (Group A) were alive on arrival and six patients (Group B) resumed heartbeats after cardiopulmonary resuscitation (CPR). The survival times for Groups A and B ranged from 3 to 72 h. The remaining 22 patients (Group C) did not survive cardiopulmonary arrest on arrival (CPAOA). Systemic distribution of lidocaine was measured in nine patients from Group C. The liver-to-kidney lidocaine ratios and cerebrum-to-cerebrospinal fluid lidocaine ratios were: Group A, 0.1-0.7 and 1.4-3.6, respectively; Group B, 0.2-0.8 and 1.2-2.3, respectively; Group C, 0.1-17 and 0.2-1.0, respectively. MEGX was detected in all blood samples from Group A and only two samples from Group B. No MEGX was detected in samples from Group C. Our results indicate that the absorption of tracheal lidocaine during natural circulation results in a cerebrum-to-cerebrospinal fluid lidocaine ratio of 1.2 or more, whereas absorption during artificial circulation by cardiac massage gives a ratio of 1.0 or less. The cerebrum-to-cerebrospinal fluid lidocaine ratio may be a more useful index to estimate circulatory dynamics of patients during CPR than the liver-to-kidney lidocaine ratio. MEGX was not a useful parameter for monitoring circulatory changes during cardiac massage.     

Tissue distribution of intubation-related lidocaine in brain-dead patients

Tissue distribution of lidocaine that was used for endotracheal intubation during cardiopulmonary resuscitation (CPR) was measured in 3 patients who were brain-dead or near brain death. Case 1 was a 69-year-old female whose heartbeat was restored by CPR but stopped 10 hours later. The lidocaine ratios of cerebrum to blood (2.04) and diencephalon to blood (1.01) were within ranges of those found in non-brain-dead patients. Case 2 was a 77-year-old female whose heart resumed beating after CPR but stopped 66 hours later. The lidocaine ratios of cerebrum to blood (5.69), diencephalon to blood (18.7), and cerebellum to blood (11.3) were much higher than those in non-brain-dead patients. Case 3 was a 48-year-old male who had cardiopulmonary arrest following an acute subarachnoid hemorrhage. His heart resumed beating after resuscitation but ceased beating 114 hours after admission. Lidocaine was detected only from the cerebrum, cerebellum, and blood clots in the superior sagittal sinus at levels of 0.028, 0.024, and 0.007 mug/g, respectively. Tissue distribution of intubation-related lidocaine in brain-dead patients is useful as supplementary data for reviewing hemodynamic changes in their brains during medical treatment.     

Fatal high cervical spinal cord injury in an automobile accident complicating os odontoideum

We report a case where spinal instability from incomplete fusion of the dens of C2 (os odontoideum) allowed anterior displacement of the skull and first cervical vertebra following right frontal impact against the A pillar in an automobile accident. Resultant crushing and laceration of the spinal cord occurred at the level of C1 and C2. Without either radiographic investigation or detailed examination of the spine, the fatal injury might have been overlooked and death attributed to acute alcoholic poisoning because the blood alcohol level was .613%.     

Sudden death from saccular laryngeal cyst

Laryngeal cysts are benign, uncommon lesions of the larynx that have been reported on rare occasions to cause sudden death in infants and adults by acute airways obstruction. In this report, we document the sudden death of a 36-year-old woman from a previously undiagnosed, asymptomatic laryngeal saccular cyst that presented with acute, and consequent fatal, airway obstruction. Difficulty during intubation, both in theater and in emergency settings, is a frequent presenting problem. This can have significant medicolegal implications in determining possible negligence. The diagnosis, classification, and management of such cysts, and their importance to both the forensic pathologist and clinicians are discussed.     

Airway obstruction by laryngeal masses in sudden and homicidal deaths

We present two cases of autopsy detection of laryngeal masses with medico-legal implications. The first is a 56-year-old man who died suddenly of asphyxia due to upper airway obstruction caused by a large glosso-epiglottic retention cyst and glottic oedema. Hypothesis of medical liability was raised, due to delayed tracheotomy as the result of repeated failed attempts at oral intubation by various physicians. Difficult oral intubation due to the presence of a laryngeal mass in an asphyxiating subject requires rapid tracheotomy. The second case deals with a 43-year-old woman who died of asphyxia due to airway obstruction, as a result of injury of a cavernous laryngeal haemangioma after homicidal manual strangulation, with severe haemorrhagic infiltration of the surrounding soft tissues. Damage to laryngeal/hypopharyngeal masses should be considered as a possible sign of manual strangulation, as well as neck skin bruises/abrasions and laryngeal haemorrhages.     

大鼠实验性脑梗死后早期CT表现的法医学研究

目的探讨24h内脑梗死CT值的变化与梗死时间的关系以及CT表现。方法采用线栓法制作大鼠大脑中动脉梗死模型,于梗死后2、3、4、6、8、12、24h进行头颅CT冠状位扫描。观察CT图像,测量两侧大脑半球对称部位的CT值,并求出两者的差值。结果线栓法大鼠脑梗死后最早于3h肉眼即可辨别梗死灶,其患侧CT值与健侧有显著性差异,且脑梗死健、患侧CT值的差值与时间呈直线正相关。结论血管栓塞引起的脑梗死最早于梗死发生后3h即可诊断,并可通过脑梗死两侧CT值的差值的计算来推断脑梗死发生的时间。     

Sudden, unexpected death due to massive, nontraumatic intra-abdominal hemorrhage in association with cirrhosis of the liver

Hemoperitoneum is usually due to rupture, laceration, or perforation of a blood vessel or organ. The author describes three deaths due to massive intra-abdominal hemorrhage, all in alcoholics with cirrhosis of the liver, in which no source for the bleeding was found. One of the three individuals, who was briefly hospitalized, showed evidence of a disseminated intravascular coagulopathy (DIC). In the author's opinion, this is the most likely cause of the intra-abdominal hemorrhage in the two other cases and is related to the cirrhosis of the liver.     

Cardiac laceration and pericardial tamponade due to cardiopulmonary resuscitation after myocardial infarction.

Complications of cardiopulmonary resuscitation (CPR), such as rib fractures and pneumothorax, are not uncommon. The authors report the case of a 69-year-old woman who underwent surgery for a perforated duodenal ulcer. Eighteen hours postoperatively she sustained a cardiac arrest; vigorous resuscitation efforts, using advanced cardiac life-support procedures, failed. At autopsy, she had 350 mL of fresh blood in her pericardial sac, which had caused cardiac tamponade. Three ribs were fractured at the left sternal border. Directly underneath the fractured ribs were a 0.4-cm laceration of the pericardium and an accompanying 0.7-cm laceration of the left ventricle. There was an acute thrombus in the left anterior descending artery. Microscopic examination of the heart showed acute infarction of the left ventricle in the vicinity of the laceration. This case demonstrates that vigorous CPR performed on an acutely infarcted heart can result in lethal cardiac laceration and tamponade.