Spike generation from dorsal roots and cutaneous afferents by hypoxia or hypercapnia in the rat in vivo.
The present study aimed at investigating the responsiveness of different parts of the primary afferent neurones to a brief hypoxia, hypercapnia or ischaemia under in vivo conditions. Action potentials were recorded in separate groups of anaesthetized rats from (i) the peripheral end of the central stump of the cut L3, L4 or L5 dorsal root (dorsal root preparation); (ii) the central end of the peripheral stump of the cut saphenous nerve (saphenous-receptor preparation); (iii) the distal end of a segment of the saphenous nerve cut at both ends (axon preparation). In paralysed animals interruption of artificial ventilation for 20-60 s elicited or increased the frequency of action potentials in both the dorsal root and saphenous-receptor preparations. Activation of these preparations was also achieved by inspiration of gas mixtures containing 10-0% oxygen (mixed with nitrogen) or 20-50% carbon dioxide (mixed with oxygen) which elicited in the blood a decrease in PO2 or an increase in PCO2 with a fall in pH. Occlusion of the femoral artery for 3 min also caused spike generation in the saphenous-receptor preparations with little alteration in blood pressure. All these stimuli failed to evoke action potentials in the axon preparations. Systemic (300 mg kg-1 s.c.) or perineural (2%) capsaicin pretreatment failed to inhibit the effect of hypoxia, hypercapnia or ischaemia, indicating a significant contribution of capsaicin-insensitive neurones to the responses. It is concluded that central and peripheral terminals but not axons of primary afferent neurones are excited by a brief hypoxia or hypercapnia and the peripheral terminals by a short local ischaemia as well. Excitation of central terminals by hypoxia or hypercapnia revealed in this way an antidromic activation of dorsal roots in response to natural chemical stimuli. (+info)
A resuscitated case from asphyxia by large bronchial cast.
A 62-year-old woman with bronchiectasis suffered from asphyxia due to a large bronchial cast that obstructed the bronchial tree. Immediate bronchoscopic suction of a bronchial cast of 17 cm in length through the intubated tube relieved the patients without any complications. Large bronchial casts appear to be rare in this century but it should be considered in patients with acute exacerbation of excessive sputa not only in patients with asthma or allergy but also in patients with respiratory tract infection. (+info)
Unnatural sudden infant death.
AIM: To identify features to help paediatricians differentiate between natural and unnatural infant deaths. METHOD: Clinical features of 81 children judged by criminal and family courts to have been killed by their parents were studied. Health and social service records, court documents, and records from meetings with parents, relatives, and social workers were studied. RESULTS: Initially, 42 children had been certified as dying from sudden infant death syndrome (SIDS), and 29 were given another cause of natural death. In 24 families, more than one child died; 58 died before the age of 6 months and most died in the afternoon or evening. Seventy per cent had experienced unexplained illnesses; over half were admitted to hospital within the previous month, and 15 had been discharged within 24 hours of death. The mother, father, or both were responsible for death in 43, five, and two families, respectively. Most homes were disadvantaged--no regular income, receiving income support--and mothers smoked. Half the perpetrators had a history of somatising or factitious disorder. Death was usually by smothering and 43% of children had bruises, petechiae, or blood on the face. CONCLUSIONS: Although certain features are indicative of unnatural infant death, some are also associated with SIDS. Despite the recent reduction in numbers of infants dying suddenly, inadequacies in the assessment of their deaths exist. Until a thorough postmortem examination is combined with evaluation of the history and circumstances of death by an experienced paediatrician, most cases of covert fatal abuse will go undetected. The term SIDS requires revision or abandonment. (+info)
What is the leading cause of infant mortality? A note on the interpretation of official statistics.
OBJECTIVES: According to vital statistics reports, congenital malformation is the leading cause of infant death in the United States and accounts for a much greater proportion of infant mortality than does premature birth. The purpose of this study was to examine the potential underestimation of prematurity-related mortality in current vital statistics reports. METHODS: National mortality data from 1985, 1991, and 1996 were analyzed. RESULTS: The official statistics significantly understate the role of prematurity-related mortality. An alternative etiology-based classification designates prematurity as the underlying cause in approximately one third of all infant deaths. CONCLUSIONS: Although no single scheme is suitable for every objective, analysts and policymakers should recognize the degree to which technical classification practices can influence the apparent importance of various causes of death. (+info)
Intra-alveolar haemorrhage in sudden infant death syndrome: a cause for concern?
BACKGROUND: The "Back to Sleep" campaign in 1991 resulted in a dramatic decrease in the incidence of sudden infant death syndrome (SIDS). The proportion of presumed SIDS deaths being actually suspicious deaths from airway obstruction is likely to have become relatively greater. There is usually little pathological evidence to suggest smothering, but intra-alveolar haemorrhage appears to be more prominent in cases where interference with the airway is suspected. AIM: To attempt to quantify intra-alveolar haemorrhage to see whether it could be used as a marker to distinguish between smothering/overlaying and SIDS. METHODS: Intra-alveolar haemorrhage was quantified using digital image analysis on haematoxylin/eosin stained sections taken from the lungs of 62 consecutive infants who had died suddenly and unexpectedly. Cases were initially classified according to the original cause of death. After quantitation, the case histories were critically reviewed. Three pathologists independently made microscopic assessments of the degree of intra-alveolar haemorrhage in the first 24 cases to see whether these accurately reflected the quantitative results. RESULTS: 73% of those infants with a history suggesting possible involuntary overlaying and 45% of those with a history suspicious of smothering had significant intra-alveolar haemorrhage (> 5% of total lung surface area assessed). From the history, the cause of death in 11 cases initially classified as SIDS would better have been given as "Unascertained." Simple microscopic assessments underestimated the true extent of the haemorrhage in 33% (8/24). CONCLUSIONS: If a moderate degree (at least 5%) of pulmonary parenchymal haemorrhage is observed, this may be an indicator of airway obstruction for a significant period, either from overlaying or possibly smothering. The diagnosis of SIDS may be being used inappropriately in such cases. (+info)
Hypothermia during reperfusion after asphyxial cardiac arrest improves functional recovery and selectively alters stress-induced protein expression.
This study examined whether prolonged hypothermia induced 1 hour after resuscitation from asphyxial cardiac arrest would improve neurologic outcome and alter levels of stress-related proteins in rats. Rats were resuscitated from 8 minutes of asphyxia resulting in cardiac arrest. Brain temperature was regulated after resuscitation in three groups: normothermia (36.8 degrees C x 24 hours), immediate hypothermia (33 degrees C x 24 hours, beginning immediately after resuscitation), and delayed hypothermia (33 degrees C x 24 hours, beginning 60 minutes after resuscitation). Mortality and neurobehavioral deficits were improved in immediate and delayed hypothermia rats relative to normothermia rats. Furthermore, both immediate and delayed hypothermia improved neuronal survival in the CA1 region of the hippocampus assessed at 14 days. In normothermia rats, the 70-kDa heat shock protein (Hsp70) and 40-kDa heat shock protein (Hsp40) were increased within 12 hours after resuscitation in the hippocampus. Delayed hypothermia attenuated the increase in Hsp70 levels in the hippocampus but did not affect Hsp70 induction in the cerebellum. Hippocampal expression of Hsp40 was not affected by hypothermia. These data indicate that prolonged hypothermia during later reperfusion improves neurologic outcome after experimental global ischemia and is associated with selective changes in the pattern of stress-induced protein expression. (+info)
Suffocated prone: the iatrogenic tragedy of SIDS.
Epidemiologic research has shown that prone sleeping is a major risk factor for sudden infant death syndrome (SIDS). In a public health review from Sweden, we explored the historical background of the SIDS epidemic, starting with the view of the Catholic Church that sudden infant deaths were infanticides and ending with the slowly disseminated recommendation of a prone sleeping position during the 1960s, 1970s, and 1980s. The story of the SIDS epidemic illustrates a pitfall of preventive medicine--the translation of health care routines for patients to general health advice that targets the whole population. False advice, as well as correct advice, may have a profound effect on public health because of the many individuals concerned. Preventive measures must be based on scientific evidence, and systematic supervision and evaluations are necessary to identify the benefits or the harm of the measures. The discovery of the link between prone sleeping and SIDS has been called a success story for epidemiology, but the slow acceptance of the causal relationship between prone sleeping and SIDS illustrates the weak position of epidemiology and public health within the health care system. (+info)
"Bystander" chest compressions and assisted ventilation independently improve outcome from piglet asphyxial pulseless "cardiac arrest".
BACKGROUND: Bystander cardiopulmonary resuscitation (CPR) without assisted ventilation may be as effective as CPR with assisted ventilation for ventricular fibrillatory cardiac arrests. However, chest compressions alone or ventilation alone is not effective for complete asphyxial cardiac arrests (loss of aortic pulsations). The objective of this investigation was to determine whether these techniques can independently improve outcome at an earlier stage of the asphyxial process. METHODS AND RESULTS: After induction of anesthesia, 40 piglets (11.5+/-0.3 kg) underwent endotracheal tube clamping (6.8+/-0.3 minutes) until simulated pulselessness, defined as aortic systolic pressure <50 mm Hg. For the 8-minute "bystander CPR" period, animals were randomly assigned to chest compressions and assisted ventilation (CC+V), chest compressions only (CC), assisted ventilation only (V), or no bystander CPR (control group). Return of spontaneous circulation occurred during the first 2 minutes of bystander CPR in 10 of 10 CC+V piglets, 6 of 10 V piglets, 4 of 10 CC piglets, and none of the controls (CC+V or V versus controls, P<0.01; CC+V versus CC and V combined, P=0.01). During the first minute of CPR, arterial and mixed venous blood gases were superior in the 3 experimental groups compared with the controls. Twenty-four-hour survival was similarly superior in the 3 experimental groups compared with the controls (8 of 10, 6 of 10, 5 of 10, and 0 of 10, P<0.05 each). CONCLUSIONS: Bystander CPR with CC+V improves outcome in the early stages of apparent pulseless asphyxial cardiac arrest. In addition, this study establishes that bystander CPR with CC or V can independently improve outcome. (+info)