Cases reported "Heart Arrest"

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1/24. Cardiac syncope secondary to glossopharyngeal neuralgia--effectively treated with carbamazepine.

    A 64-year-old male with glossopharyngeal neuralgia, cardiac asystole and grand mal seizures has been relieved of his attacks by intake of 400 mg of carbamazepine per day over a 4-year period. Simultaneous EEG-EKG recordings before and after drinking water document the diagnosis.
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2/24. Successful resuscitation of a child with severe hypothermia after cardiac arrest of 88 minutes.

    A 4-year-old boy broke through the ice of a frozen lake and drowned. The boy was extricated from the icy water by a rescue helicopter that was dispatched shortly after the incident. Although the boy was severely hypothermic, no cardiac response could be induced with field resuscitation measures, including intubation, ventilation, suction, and cardiopulmonary resuscitation. On admission, the primary findings included fixed, nonreacting pupils and asystole. The first core temperature measured was 19.8 degrees C (67.6 degrees F). During active, external warming, the first ventricular beats were observed 20 minutes after admission, and changed 10 minutes later to a sinus rhythm. Continuous monitoring included repeated arterial blood gas and electrolyte tests; prophylaxis for cerebral edema was performed with hyperventilation and administration of sodium Brevimytal and dexamethasone. Seventy minutes after admission, hemodynamics stabilized and the boy was transferred to the pediatric intensive care unit (PICU), where active external warming was continued to raise the core temperature at a rate of 1 degree C/hour. adult respiratory distress syndrome developed, and the boy had to be ventilated in the PICU for 10 days. He was discharged home after another two weeks. He recovered fully. The rapid heat loss with the induction of severe hypothermia (< 20 degrees C; 68 degrees F) was the main reason for survival in this rare event of a patient with cardiac arrest lasting 88 minutes after accidental hypothermia.
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3/24. Postpartum clostridium sordellii infection associated with fatal toxic shock syndrome.

    Clostridium bacteria are anaerobic Gram positive spore-form-ing bacilli, known to cause distinct clinical syndromes such as botulism, tetanus, pseudomembranous colitis and myonecrosis. The natural habitats of Clostridium species are soil, water and the gastrointestinal tract of animals and humans. In 5-10% of all women, Clostridium species are also found to be normal inhabitants in the microbial flora of the female genital tract. In case of a non-sexually transmitted genital tract infection, Clostridium species are isolated in 4-20%, and clostridium welchii seems to be the most common isolate. clostridium sordellii is rarely encountered in clinical specimens (1% of Clostridium species), but it has been described as a human pathogen with fatal potential. Two toxins, a lethal and a hemorrhagic (that antigenically and pathophysiologically appear similar to clostridium difficile toxins B and A, respectively) are responsible for this potential. Reviewing the obstetric literature, only six cases of postpartum endometritis caused by C. sordellii, are described - all being fatal. In addition, one lethal case of spontaneous endometritis resulting from C. sordellii is reported. The clinical aspects of these cases include: - sudden onset with influenza-like symptoms in previously healthy women - progressive refractory hypotension - local and spreading tissue edema - absence of fever Laboratory findings include: - marked leukocytosis - elevated hematocrit. This paper reports the seventh fatal postpartum C. sorlellii associated toxic shock syndrome - the first recognized in scandinavia.
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4/24. Cold water submersion and cardiac arrest in treatment of severe hypothermia with cardiopulmonary bypass.

    In the paediatric population, submersion injury with drowning or near-drowning represents a significant cause of morbidity and mortality. This study reviews retrospectively our own experiences and the literature on the use of cardiopulmonary bypass (CPB) to rewarm paediatric victims of cold water submersion who suffer severe hypothermia (<28 degrees C) and cardiac arrest (asystole or ventricular fibrillation). In addition to three children treated at our institution, nine other victims were found in the literature. In this cohort of 12 children aged between 2 and 12 years, there was a tendency to better outcome with lower core temperature at the beginning of extracorporeal circulation (mean temperature in nine survivors, 20 degrees C; in three non-survivors, 25.5 degrees C). The lowest temperature survived was 16 degrees C. Neither base excess, pH nor serum potassium levels were reliable prognostic factors. The lowest base excess in a survivor was -36.5 mmol/l, the lowest pH 6.29. We consider CPB as the method of choice for resuscitation and rewarming of children with severe accidental hypothermia and cardiac arrest (asystole or ventricular fibrillation). Compared with adults, children, especially smaller ones, require special consideration with regard to intravenous cannulation as drainage can be inadequate using femoral-femoral cannulation. In hypothermic children we advocate, therefore, emergency median sternotomy. Until more information regarding prognostic factors are available, children who are severely hypothermic and clinically dead after submersion in cold water--even if for an unknown length of time--should receive cardiopulmonary resuscitation (CPR) and be transported without delay to a facility with capabilities for CPB instituted via a median sternotomy.
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5/24. Prehospital cardiac arrest in diabetic ketoacidemia: why brain swelling may lead to death before treatment.

    An adolescent is reported with type 1 diabetes mellitus and diabetic ketoacidemia (DKA) who died from brain herniation prior to treatment with intravenous fluids and intravenous insulin. The pathophysiology of raised intracranial pressure (ICP) and water intoxication is discussed. As DKA evolves, water and electrolyte losses are replaced by very hypotonic fluids taken orally, leading to a physiologic excess of free water that would cause brain swelling prior to treatment. central nervous system acidosis may interfere with normal compensatory mechanisms that help prevent small increases in ICP. The pathophysiology of pre-treatment brain swelling has important implications for rehydration with intravenous fluids and treatment with insulin. Prevention of DKA is paramount as well as complete postmortem evaluation of patients who die from this disease.
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6/24. Mechanism of sudden cardiac arrest while swimming in a child with the prolonged QT syndrome.

    We describe the abrupt sequence of events resulting in cardiac arrest while swimming in a 12-year-old with long qt syndrome. diving into cold water resulted in an irregular cardiac rhythm and further prolongation of the QT interval, followed by a premature ventricular complex, which initiated pulseless ventricular tachycardia (rate >300/minute). The transition from sinus rhythm to ventricular tachycardia occurred in <5 seconds and was followed by a successful implantable cardioverter-defibrillator rescue shock.
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7/24. cardiopulmonary resuscitation of a near-drowned child with a combination of epinephrine and vasopressin.

    OBJECTIVE: To report a cardiopulmonary resuscitation attempt in a 20-month-old child employing a combination of vasopressin and epinephrine. DESIGN: Case report. SETTING: Out-of-hospital cardiopulmonary resuscitation. PATIENT: A 20-month-old child found in cardiac arrest after submersion. INTERVENTIONS AND RESULTS: Dispatcher-assisted basic life support was initiated immediately after pulling the child out of the water. The emergency medical service crew arrived approximately 6 mins later and found a hypothermic, cyanotic child in cardiocirculatory arrest. The first electrocardiogram showed sinus bradycardia. After intubation and administration of epinephrine and atropine with no effect, an intravenous bolus of 0.2 mg of epinephrine and 10 IU of vasopressin resulted in restoration of spontaneous circulation. The boy was flown to a hospital and was discharged 23 days later to a rehabilitation facility. He returned home 6 months after the accident, where further rehabilitation efforts are pending. CONCLUSION: Bystander cardiopulmonary resuscitation, early and aggressive advanced life support, rewarming, and the combination of intravenous epinephrine and vasopressin were associated with sustained return of spontaneous circulation following hypothermic submersion-associated cardiac arrest.
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8/24. Complete neurological recovery following delayed initiation of hypothermia in a victim of warm water near-drowning.

    Induced hypothermia has been demonstrated to improve outcome following cardiac arrest and is now widely endorsed. However, the optimal method of cooling and the identification of patients most likely to benefit from this therapy remains to be determined. We report a patient in whom there was a long delay in return of spontaneous circulation (at least 45 min) and the initiation of induced hypothermia (12 h) who made an almost complete neurological recovery following cardiac arrest from warm-water near-drowning.
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9/24. Problems and complications with cold-water rescue.

    A case description is presented of a 9-member rowing team whose scull swamped on a small lake in victoria, canada, because of a sudden winter storm, which immersed them in 4 degrees C water for 50 minutes until a small rescue boat found them in darkness. Another 13 minutes of cold exposure in 6.7 degrees C air occurred during boat transport to waiting ambulance paramedics. Two rowers died, one from severe hypothermia and the other from drowning as a consequence of cold incapacitation and hypothermia. The 2 coldest rowers, who were transported 8 km to a major hospital, arrived with rectal temperatures of 23.4 degrees C and 25 degrees C; the first was asystolic and the second was unconscious and in sinus bradycardia. Analysis of all the circumstances of this incident provided an opportunity to observe a continuum of responses in a heterogeneous group of rowers at risk of severe hypothermia. Several practical lessons concerning cold-water survival, rescue, and treatment can be learned. The effects of low body mass were associated with greater cooling rate. Diminished neuromuscular performance in the periphery appeared to be independent of body mass. Rough handling during moving of patients with marked hypothermia introduces the risk of producing ventricular fibrillation or cardiac arrest. Unconscious, nonshivering hypothermia victims who are rescued and insulated from cold could have a further afterdrop of 3 degrees C to 4 degrees C. During transport to a hospital, the use of heating devices concentrating on core regions may increase the chance of successful treatment in the hospital. cardiopulmonary bypass may be indicated for severely hypothermic patients in asystole.
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10/24. Historical perspectives on anesthetic-related cardiac arrest and resuscitation.

    Contemporary interest in resuscitation was historically related to anesthetic death. Primitive techniques of anesthetic administration, loss of airway control, and psychologically influenced sudden death contributed to unanticipated respiratory and cardiac arrest. airway obstruction has remained the principal factor in asphyxial death, necessitating crucial preservation of respiratory function during induction of anesthesia. Early, disorganized overdose and arrest interventions included: application of cold water, manual artificial respiration, heat, friction and galvanic battery application. cardiopulmonary resuscitation, after years of research and experimentation became an integrated plan of attack: mouth-to-mouth ventilation and maneuvers eliminating pharyngeal obstruction were proven effective; internal and external cardiac massage was incorporated and definitive drug therapy began with epinephrine, strychnine, caffeine, carbon dioxide, amyl nitrate, coramine, metrazol and procaine. Defibrillation proved electricity converted ventricular fibrillation to normal sinus rhythm. Significant lethality still occurs from anesthetic-induced cardiac arrest, despite technological advances. Causes of operating room cardiac arrests are numerous and include sudden death syndrome. Constant vigilance distinguishes variable patient response. Immediate recognition and coordinated intervention assures success.
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