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.     

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.     

Distribution of lidocaine and disopyramide in human blood and tissue, a case report of death caused by spinal anesthesia

An 11-year-old girl was anesthetized with hyper-baric solution of lidocaine as spinal anesthesia for an appendectomy in a surgical clinic. Respiratory arrest which occurred soon after the injection, was not discovered for a period of time. Since spontaneous respiration recovered within 2 h of intensive resuscitation, the patient was transferred to a community hospital for intensive care. Ten hours after the spinal anesthesia, she died of cardiac failure. The concentration of lidocaine in the brain was 5-10 times more than that in other tissues. The relationship between the possibility of malpractice of spinal anesthesia and tissue distribution of the drug was discussed. In addition to lidocaine, a toxic amount of disopyramide, an antiarrhythmic drug, was detected in the body. The distribution of disopyramide was also estimated, and the pharmacokinetics of disopyramide in plasma and tissues were studied experimentally in rats.     

Iatrogenic tracheal laceration causing asphyxia

Endotracheal intubation is a simple, rapid, and safe technique that is being used as a standard procedure for airway management. However, airway injury during endotracheal intubation could be a significant source of morbidity or even mortality for patients and a source of liability for physicians as well. We report an unusual case of fatal tracheal occlusion by intraluminal blood clot complicating endotracheal intubation. The patient, a 62-year-old woman, with renovascular hypertension and incipient renal failure was scheduled for renal autotransplantation. The surgery was uneventful but the postoperative course was complicated with a lethal airway obstruction. At autopsy a linear longitudinal tracheal laceration was identified with an intraluminal blood clot obstructing the tracheal lumen. Tracheal laceration as a cause of death is a rare and potentially fatal complication of endotracheal intubation with intratracheal bleeding, clot formation, tracheal occlusion, and subsequent asphyxia.     

Tissue distribution of lidocaine after fatal accidental injection

The accidental death of a 64-year-old heart patient as a result of the injection of an incorrect dose of lidocaine is presented. The attending nurse inadvertently administered an intravenous bolus of 10 mL of 20% lidocaine (2g). The patient should have received 5 mL of 2% lidocaine (0.1 g). Such iatrogenic overdoses of lidocaine arise from confusion between prepackaged dosage forms. Lidocaine concentrations (mg/L or mg/kg were: blood, 30; brain, 135; heart, 106; kidney, 204; lung, 89; spleen, 115; skeletal muscle, 20; and adipose, 1.3. The results indicate that even during cardiopulmonary resuscitation as much as 38% of the administered dose of lidocaine may be found in poorly perfused tissue such as skeletal muscle and adipose.     

A case of homicide by lethal injection with lidocaine

This report describes a homicide by overdosage with lidocaine. The decedent, a 32-year-old male hospitalized for a lengthy period with acute intermittent porphyria and chronic pancreatitis, suffered apparent asystole and seizure. Failed resuscitation preceded death. A forensic autopsy was conducted based upon suspicions of alleged patient mistreatment by one of the attending nurses. Toxicological analyses revealed the presence of lidocaine in blood, liver, kidney, brain, and heart at 22.2 mg/L and 43.6, 28.3, 23.1, and 13.1 mg/kg, respectively. Also present were diazepam, phenytoin, and promethazine. Both diazepam and phenytoin had been administered during resuscitation, but lidocaine had not. The cause of death was determined to be ventricular arrhythmia precipitated by lidocaine overdosage. The administered dose was calculated to have been approximately 1500 mg. The manner of death was determined to be homicide. The nurse was arrested and subsequently tried for murder by administering a lethal quantity of lidocaine.     

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.     

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.     

Reporting a fatality during tumescent liposuction

Deaths of patients during elective surgery have drawn attention to the danger of anesthesia. Tumescent local anesthesia is subcutaneous infiltration of large volumes of dilute lidocaine with epinephrine to produce vasoconstriction while delivering anesthesia over large areas without lidocaine toxicity. This report documents the case of a 38-year-old woman who attended an outpatient clinic to undergo liposuction of the abdomen and bilateral hips and thighs. According to one witness, around 30 min after anesthesia administration, the victim suffered an episode of tonic–clonic convulsion. When the emergency medical services arrived the patient was in asystole. She died in spite of attempted cardiopulmonary resuscitation. The patient had no significant past medical history including no history of allergies or any known complications with anesthesia. A complete autopsy was performed and possible causes of death such as myocardial infarction, aspiration of food or foreign body, and pulmonary embolism were discarded. Anaphylactic shock was considered a possible but unlikely explanation for the fatality. Toxicological analyses revealed the presence of lidocaine and mepivacaine in heart blood, at concentrations of 4.9 and 16.2 mg/L, respectively. All drugs involved in the case were detected using gas chromatography with nitrogen–phosphorus detector and confirmed using gas chromatography–mass spectrometry full scan mode after solid-phase extraction using Chem-Elut columns. An additional high-performance liquid chromatography coupled to diode-array detection screening also obtained the same results. Based on the autopsy findings, case history, and toxicology results, the forensic pathologists ruled that the cause of death was an overdose of local anesthetic agents. The Court of Law ruled the death as an involuntary homicide due to gross negligence.     

The deadly broomstick: an unusual missile injury to the neck

A 51-year-old man was struck by the tip of a broomstick weighing 1000 g at the left side of the neck, upon which he collapsed. Intense but delayed cardiopulmonary resuscitation restored the circulation roughly 30 minutes after the incident. Upon admittance to a nearby hospital, an extensive hypoxic cerebral damage was diagnosed. Death due to the severe cerebral damage occurred 5 hours after the incident. An autopsy demonstrated a severe subcutaneous traumatization of the left side of the neck, with a hemorrhage compressing the carotid bifurcation. A prolonged excitation due to this ongoing compression of the baroreceptors in the carotid sinus was assumed to have led to a cardiac arrest. In this case report, the authors discuss the underlying pathophysiology of this potentially lethal and rare reflexogenic incident also known as the Hering reflex and discuss possible therapeutic measures.     

Flail Chest Following Failed Cardiopulmonary Resuscitation

Following the death of a woman with blunt force chest trauma, the question was asked how common was the finding at autopsy of a flail chest in decedents after failed cardiopulmonary resuscitation. It was suggested in court that this was an uncommon occurrence. To address this issue, autopsy cases in adults (>18 years) with rib fractures attributable to cardiopulmonary resuscitation were taken from the files of Forensic Science SA over a 7‐year period from 2008 to 2014. Flail chest injuries were defined as those arising from fractures at two sites in at least three consecutive ribs. From 236 cases with rib fractures attributed to resuscitation, a total of 43 flail chest injuries were found in 35 cases (14.8%). The majority occurred in the 60‐79‐year‐old age group. These data suggest that flail chest injuries are a more common sequelae of cardiopulmonary resuscitation than has been previously appreciated in autopsy cases, particularly in the elderly.     

Death during percutaneous transluminal coronary angioplasty (PTCA) and the medicolegal aspects

Coronary embolisation is a very rare complication of the clinically widespread method of percutaneous transluminal coronary angioplasty (PTCA). The well-documented case of a 64-year-old male patient is presented comparing angiographic and morphological findings. The occluded left anterior descending artery (LAD) was successfully dilated during PTCA. Simultaneously the circumflex artery showed acute occlusion. The patient fell into cardiac shock and died after attempted resuscitation and agonal installation of extracorporeal circulation. The autopsy revealed severe residual stenosis of the proximal LAD by parietal thrombosis and occlusion of the proximal circumflex artery by an unattached intraluminal thrombus (0.8 x 0.3 x 0.2 cm) which had been dislocated during PTCA. Autopsy thus confirmed the clinical presumption of coronary embolism and, in addition, disclosed a previously unknown perforation of the femoral artery which had occurred during agonal installation of extracorporeal circulation and contributed to death via severe retroperitoneal hemorrhage. The case is discussed under the aspects of clinical quality control by forensic pathological investigations.     

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.     

Complete Cardiac Rupture Associated with Closed Chest Cardiac Massage: Case Report and Review of the Literature

Chest skeletal injuries are the most frequent complications of external chest massage (ECM) during cardiopulmonary resuscitation, but heart and great vessels lacerations that are indeed very rare. We report the case of a 35‐year‐old workman who collapsed and underwent ECM by his co‐workers for almost 30 min. At autopsy, no external injuries, fractures or bruises of the ribs or sternum, were observed. A hemopericardium with a rupture of the heart was found, with no signs of pre‐existent cardiac disease. Bruises of thoracic aortic wall, lung petechiae, a contusion of the liver, and bruises of lumbar muscles were found. The cause of death was due to sudden cardiac death with an extensive cardiac rupture. This is an unusual report of massive heart damage without any skeletal or muscle chest injuries, secondary to cardiopulmonary resuscitation. This kind of cardiac lesions may be considered when thoracic–abdominal trauma, or medical history, is unclear.     

Concentrations of lidocaine and monoethylglycylxylidide (MEGX) in lidocaine associated deaths

Concentrations of lidocaine and MEGX were determined in a variety of tissues and other samples collected at autopsy. In 13 of the cases examined in which lidocaine was associated with death, tissue concentrations were greater than 15 mg/kg. Tissue concentrations in other patients treated with lidocaine were significantly lower.     

利多卡因在蛛网膜下腔麻醉致死犬体内的分布

目的 观察利多卡因蛛网膜下腔致死犬体内的分布及脊髓液、脊髓与血液中利多卡因含量的比值。方法薄层扫描法检测血、脊髓液、侧脑室液、各节段脊髓和各脏器组织中利多卡因含量。结果 蛛网膜下腔麻醉致死犬脊髓液、各节段脊髓、脑、血液和其它各脏器中利多卡因含量分别为485.6±51.5μg/ml、226.8±35.2-353.8±44.0μg/g、44.9±11.51μg/g、40.3±6.5μg/ml和13.5±13.7-38.0±9.8μg/g。脊髓液与血液中利多卡因含量之比为12.4±2.7,各节段脊髓与血液之比为5.7±0.9-9.0±2.6。结论 蛛网膜下腔麻醉致死犬脊髓液中利多卡因含量最高,脊髓中次之,血液和其它组织中含量较低。脊髓液/血液、脊髓/血液比值平均可达12.4和5.7-9.0。     

An unusual case of accidental poisoning: fatal methadone inhalation

In this report, the authors present a case of unusual, accidental methadone intoxication in a 40-year-old man, who had inhaled methadone powder. The drug dealer was a pharmacy technician; methadone had been stolen from a pharmacy and sold as cocaine. After having inhaled methadone powder, he suffered cardiopulmonary arrest. He was admitted to hospital where he died after 24 h of intensive care. The autopsy revealed congestion of internal organs and cerebral and pulmonary edema. Microscopically, the heart showed no changes. The toxicological analyses performed on blood and urine taken at the hospital revealed methadone, cannabinoids, and ethanol. The blood methadone concentration was 290 μg/L. The urine methadone concentration was 160 μg/L. Midazolam and lidocaine, which were administered to the patient at the hospital, were also detected in the blood. The cause of death was determined to be methadone intoxication. The literature has been reviewed and discussed. To date, and to our knowledge, only very few cases of accidental death resulting from methadone inhalation have been described up to the case presented herein.     

Postmortem atropine concentrations in resuscitation cases

The medications used during resuscitation are often in and of themselves toxic. Several reports have been published regarding toxicities of these drugs, including lidocaine, procainamide, and atropine. But how does a forensic pathologist or toxicologist differentiate a possible intoxication from therapeutic or resuscitory use especially given that the concentrations of such drugs, when used in the setting of resuscitation, have not been studied? Concentrations of a well-known resuscitation medication, atropine, were assessed in cases where it was administered before death during attempted resuscitation in an effort to address this deficiency. A review of deaths occurring in 2009 was undertaken to identify cases where drugs known to be used during resuscitation were present on toxicological analysis. Autopsy reports and medical records were examined to determine how much atropine was administered, the timing and route of administration, the time the sample was drawn (antemortem and postmortem), the source of the sample, and the ultimate cause of death. Eighty-nine cases were identified in which atropine was given before death during attempted resuscitation and was detected in the blood on postmortem toxicological screening; 11 cases were identified in which atropine was administered before death yet was not detected on the postmortem toxicological screening. Mean age was 41 years, and there were 65 males and 35 females. The overall median dose of atropine given was 3 mg, the median difference between the time of last administration of the atropine to the time of death (or draw for antemortem samples) was 15 minutes, and the median atropine concentration was 0.1 mg/L. Analysis failed to reveal significant differences in the atropine concentration based on the route of administration (intravenous or intraosseus), the cause of death, or the time since administration (within the first 2 hours). Analysis did reveal a difference between the atropine concentrations in peripheral versus central blood sources and with prolonged postmortem interval (>24 hours) suggesting postmortem redistribution.     

Oronasal blood in sudden infant death.

Oronasal secretions are observed frequently in sudden infant death syndrome (SIDS), but overt blood is uncommonly reported. The literature on oronasal blood in sudden infant death is limited. The goal of this study was to determine the frequency of oronasal blood in sudden infant deaths and to examine possible causative factors. Oronasal blood was described in 28 (7%) of 406 cases of sudden infant death. Oronasal blood could not be attributed to cardiopulmonary resuscitation in 14 cases, including 10 (3%) of 300 cases of SIDS, 2 (14%) of 14 accidental suffocation cases, and 2 (15%) of 13 undetermined cases. Eight of the 10 infants in cases of sudden infant death were bedsharing: 5 with both parents, 2 between both parents. The infant in 1 SIDS case was from a family that had had three referrals to Child Protective Services. Oronasal blood not attributable to cardiopulmonary resuscitation occurs rarely in SIDS when the infant is sleeping supine in a safe environment. Bedsharing may place infants at risk of suffocation from overlaying. Oronasal blood observed before cardiopulmonary resuscitation is given is probably of oronasal skin or mucous membrane origin and may be a sign of accidental or inflicted suffocation. Sanguineous secretions that are mucoid or frothy are likely of remote origin, such as lung alveoli. The use of an otoscope to establish the origin of oronasal blood in cases of sudden infant death is recommended.     

Resuscitation injuries complicating the interpretation of premortem trauma and natural disease in children

Minor soft tissues injuries are common in both adults and children who have had cardiopulmonary resuscitation (CPR). Potentially life-threatening injuries are rare. The pre-arrest history in a resuscitated adult often assists the pathologist to interpret autopsy findings. In contrast, an infant or child may not have a reliable history. In this situation, it may be difficult if not impossible to distinguish resuscitation injuries from pre-existing accidental or inflicted trauma. I describe two children who had significant autopsy-documented injuries initially attributed to abuse. The State filed murder charges against the caretaker in each case. However, further history and review of the medical records suggested that resuscitation rather than pre-arrest trauma caused almost all of the injuries. The State dismissed the charges in the first case. A jury returned a "not guilty" verdict in the second. It is essential to consider the entire history and not just autopsy findings when performing a death investigation.