TREATMENT OF CLOSED HEAD INJURIES

Cerebral concussion is a physiological disturbance in the brain that follows a blow on the head. The cardinal symptom is a disturbance in consciousness varying from a complete loss of consciousness to a dazed state. The phenomenon is self-limited and completely reversible.In cerebral contusion there is actual injury to the brain. The symptoms that result vary according to the amount and location of the damage. A very small amount of damage in certain areas of the brain may be fatal, while extensive damage in other areas will be survived.Even when a patient is unconscious after a head injury, certain simple neurologic tests can be done to determine with some accuracy the extent and location of brain damage. When the patient regains consciousness, further bedside tests can be carried out to increase the accuracy of diagnosis.Careful observation of the patient at frequent intervals is necessary to judicious application of appropriate treatment. The physician must be on the alert constantly for signs of intracranial hemorrhage and should be ready to intervene surgically if necessary.In most cases of injury to the head, treatment consists of supplying to the patient elements that are necessary to maintain physiologic conditions and of combating disorders arising from specific injuries to the brain.     

TRACHEOTOMY IN BULBAR POLIOMYELITIS

Tracheotomy was performed on 181 of 351 patients with bulbar poliomyelitis. The essential indication for tracheotomy was secretional obstruction of the respiratory tract that could not be relieved by postural drainage and aspiration.Comparison of mortality rates in this series with those of previous series in which tracheotomy was not done in the presence of similar indications, suggests that the procedure may be life-saving in a considerable percentage of cases.Outside the respirator the tracheotomy can be done with or without the aid of the bronchoscope or endotracheal anesthesia tube. When done inside the opened respirator the Bennett flow-sensitive positive pressure machine should be used to supply oxygen to the patient while the respirator is not operating.     

Oxygen radicals in the adult respiratory distress syndrome, in myocardial ischemia and reperfusion injury, and in cerebral vascular damage

Recent work suggests that oxygen radicals may be important mediators of damage in a wide variety of pathologic conditions. In this review we consider the evidence supporting the participation of oxygen radicals in the adult respiratory distress syndrome, in ischemia reperfusion injury in the myocardium, and in cerebral vascular injury in acute hypertension and traumatic brain injury. In the adult respiratory distress syndrome there is active sequestration of polymorphonuclear neutrophils in the pulmonary vascular system. There is evidence that activation of these neutrophils results in the production of oxygen radicals which injure the capillary membrane and increase permeability, leading to progressive hypoxia and decreased lung compliance which are hallmarks of the syndrome. In acute arterial hypertension or experimental brain injury oxygen radicals are important mediators of vascular damage. The metabolism of arachidonic acid is the source of oxygen free radical production in these conditions. In myocardial ischemia and reperfusion injury, the ischemic myocyte is "primed" for free radical production. With reperfusion and reintroduction of molecular oxygen there is a burst of oxygen radical production resulting in extensive tissue destruction. Myocardial ischemia--reperfusion injury shares in common with the other two syndromes activation of the arachidonic acid cascade and acute inflammation. Thus it would appear that the generation of toxic oxygen species may represent a final common pathway of tissue destruction in several pathophysiologic states.     

SURGICAL EMERGENCIES

Action according to preconceived plans may be life-saving at the scene of accidents involving serious injury to several persons. Severe hemorrhage and respiratory obstruction must be dealt with immediately. As the latter may not be apparent at a glance, it should be looked for specifically. Artificial respiration may be necessary. Spinal puncture is a procedure in first aid which should be carried out at the site of an accident if there are symptoms of cerebral edema or of increased cerebral pressure.Routine plans should be laid to meet the emergency of cardiac arrest on the operating table. The surgeon must be prepared to begin cardiac massage within three minutes in such instances.     

SURGICAL EMERGENCIES

Action according to preconceived plans may be life-saving at the scene of accidents involving serious injury to several persons. Severe hemorrhage and respiratory obstruction must be dealt with immediately. As the latter may not be apparent at a glance, it should be looked for specifically. Artificial respiration may be necessary. Spinal puncture is a procedure in first aid which should be carried out at the site of an accident if there are symptoms of cerebral edema or of increased cerebral pressure.Routine plans should be laid to meet the emergency of cardiac arrest on the operating table. The surgeon must be prepared to begin cardiac massage within three minutes in such instances.     

LARYNGOSPASM FROM THE ANESTHESIOLOGIST'S VIEWPOINT

Laryngeal spasm is a problem constantly confronting the anesthetist. It can be serious and may produce fatal cerebral or cardiac complications. Etiologic agents include primary vagal hypertonicity, anoxemia, and painful stimulation of whatever source.Laryngeal spasm must be differentiated from simple obstruction by the tongue or foreign bodies, epiglottic impaction, laryngeal edema, tracheal spasm and collapse, and bronchial spasm.Proper checking of the patient before anesthesia and adequate premedication with atropine or scopolamine are preventive measures of great value. Once spasm has developed the etiologic agent should be removed if possible. Other measures include intravenous administration of atropine or curare, tracheal intubation, and tracheotomy.     

Single Sustained Inflation followed by Ventilation Leads to Rapid Cardiorespiratory Recovery but Causes Cerebral Vascular Leakage in Asphyxiated Near-Term Lambs

BackgroundA sustained inflation (SI) rapidly restores cardiac function in asphyxic, bradycardic newborns but its effects on cerebral haemodynamics and brain injury are unknown. We determined the effect of different SI strategies on carotid blood flow (CaBF) and cerebral vascular integrity in asphyxiated near-term lambs.MethodsLambs were instrumented and delivered at 139 ± 2 d gestation and asphyxia was induced by delaying ventilation onset. Lambs were randomised to receive 5 consecutive 3 s SI (multiple SI; n = 6), a single 30 s SI (single SI; n = 6) or conventional ventilation (no SI; n = 6). Ventilation continued for 30 min in all lambs while CaBF and respiratory function parameters were recorded. Brains were assessed for gross histopathology and vascular leakage.ResultsCaBF increased more rapidly and to a greater extent during a single SI (p = 0.01), which then decreased below both other groups by 10 min, due to a higher cerebral oxygen delivery (p = 0.01). Blood brain barrier disruption was increased in single SI lambs as indicated by increased numbers of blood vessel profiles with plasma protein extravasation (p = 0.001) in the cerebral cortex. There were no differences in CaBF or cerebral oxygen delivery between the multiple SI and no SI lambs.ConclusionsVentilation with an initial single 30 s SI improves circulatory recovery, but is associated with greater disruption of blood brain barrier function, which may exacerbate brain injury suffered by asphyxiated newborns. This injury may occur as a direct result of the initial SI or to the higher tidal volumes delivered during subsequent ventilation.     

锌对离体鲤鱼头呼吸的抑制作用

本工作基于化学纤维工厂废水中硫酸锌含量的石超标而设计。采用改进的离体鱼头灌注法,以不同浓度的ＺｎＳＯ４．７Ｈ２Ｏ对８４个鲤鱼头进行了人工灌流,结果表明,锌的渔业水质安全下限似应以０．００２３ｍｇ／Ｌ（我国现行规定锌的渔业水质标准为０．１ｍｇ／Ｌ）为宜。     

HEADACHE OF EXTRACRANIAL ORIGIN

The cervical spine, usually regarded as a supporting structure for the head, is also an important viaduct of vessels and nerves which must function with little clearance in a congested and moving space bounded by bone. Pressure in this viaduct is an important cause of headache.The cervical foramina although apparently roomy, are constricted by cartilage, by the vertebral artery and its adnexae, and by the lateral intervertebral joints. Osteophytosis, swelling or adhesion in this constricted space almost inevitably causes painful vascular or neural disorder.In certain postures of the neck the vertebral artery is constricted or even occluded. Traction or sprain may likewise cause headache through disturbance of the vertebral arterial nerves, the posterior cervical autonomic system or the spinal accessory nerves which originate in delicate filaments from all points of the cervical spinal cord.A syndrome described by Skillern—migraine-like suboccipital and retro-orbital headache—is due to disturbance of the second cervical nerve, which communicates with the first division of the trigeminal nerve.Headache due apparently to a minor scalp contusion may really be due to irritation of a trigger area at the site of an old scalp injury.     

MEDICO-LEGAL ASPECTS OF TRAUMATIC EPILEPSY

The medico-legal problems of cranial injuries require a broad assessment of many factors, not always related to the nervous system, and a nicety of judgment in correctly evaluating the role of each factor in relation to all of them.Seizures in the period immediately after trauma are not necessarily precursors of later development of epileptic attacks. If such seizures do occur, it can be said in general, from statistical data, that the sooner they occur after injury the less the likelihood of disabling attacks later. It would seem a reasonable medical probability that if a patient has no neurological symptoms or deficit, has a normal electroencephalogram and has gone two years after injury without evidence of seizures, he will not have epilepsy.Putting a label of “post-traumatic epilepsy” on a patient, unless he is known to have had authentic seizures, may stigmatize him without warrant and lead to unjust settlement of litigation or to unreasonable compensation awards. In doubtful cases, perhaps an equitable solution of compensation for damage would be to award an insurance policy providing suitable payments if disabling seizures should develop later as a sequel of cranial injury.     

Mitochondrial respiratory chain and free radical generation in stroke

Being the second most common cause of death in the industrial countries and one of the major causes of death and disability, stroke has a great effect on public health and is the neurological disease which accounts for the largest number of hospitalizations. In order to develop new treatments, biochemical mechanisms involved in brain damage have been investigated. Among them, oxidant species generated during stroke have been implicated as critical mediators of neuronal injury in this condition, although neuroprotective roles have also been demonstrated. This review is focused on the role of the mitochondrial respiratory chain as both source and target of reactive oxygen and nitrogen species such as nitric oxide, superoxide and peroxynitrite produced in cerebral ischemia. The neuroprotective role of antioxidants or other molecules acting on the mitochondrial respiratory chain and ATP synthesis in the setting of cerebral ischemia is discussed.     

Patient-specific modeling of cardiovascular and respiratory dynamics during hypercapnia

This study develops a lumped cardiovascular–respiratory system-level model that incorporates patient-specific data to predict cardiorespiratory response to hypercapnia (increased CO₂ partial pressure) for a patient with congestive heart failure (CHF). In particular, the study focuses on predicting cerebral CO₂ reactivity, which can be defined as the ability of vessels in the cerebral vasculature to expand or contract in response CO₂ induced challenges. It is difficult to characterize cerebral CO₂ reactivity directly from measurements, since no methods exist to dynamically measure vasomotion of vessels in the cerebral vasculature. In this study we show how mathematical modeling can be combined with available data to predict cerebral CO₂ reactivity via dynamic predictions of cerebral vascular resistance, which can be directly related to vasomotion of vessels in the cerebral vasculature. To this end we have developed a coupled cardiovascular and respiratory model that predicts blood pressure, flow, and concentration of gasses (CO₂ and O₂) in the systemic, cerebral, and pulmonary arteries and veins. Cerebral vascular resistance is incorporated via a model parameter separating cerebral arteries and veins. The model was adapted to a specific patient using parameter estimation combined with sensitivity analysis and subset selection. These techniques allowed estimation of cerebral vascular resistance along with other cardiovascular and respiratory parameters. Parameter estimation was carried out during eucapnia (breathing room air), first for the cardiovascular model and then for the respiratory model. Then, hypercapnia was introduced by increasing inspired CO₂ partial pressure. During eucapnia, seven cardiovascular parameters and four respiratory parameters was be identified and estimated, including cerebral and systemic resistance. During the transition from eucapnia to hypercapnia, the model predicted a drop in cerebral vascular resistance consistent with cerebral vasodilation.     

SOME EFFECTS OF ANTIBIOTICS IN SURGERY

Although surgical mortality has decreased considerably in the antibiotic era, infectious complications still head the list of causes of death after operation.The choice of an antibiotic singly or in synergistic combinations should be governed by both the pathogenic organism and the organ involved. Allergy, toxicity and development of bacterial resistance are important limiting factors.Besides oxygen, antibiotics are indicated in dealing with localized or generalized anoxia as encountered in vascular impairment of intestinal obstruction or in shock.In acute abdominal conditions meticulous observation is required during the use of antibiotics in order to avoid dangerous delay of operation.     

Management of airway complications of burns in children.

Children who have been exposed to smoke in a confined space or who have soot or burns, however minimal, on the face should be admitted to hospital. Respiratory distress may be delayed, but if it is progressive the patient should be curarised, intubated, and mechanically ventilated. Unless ventilation continues for 48 hours, followed by 24 hours'' spontaneous respiration against a positive airway pressure, stridor and pulmonary oedema may recur. An endotracheal tube small enough to allow a leak between it and the oedematous mucosa must be passed to prevent laryngeal damage and subsequent subglottic stenosis. High humidity of inspired gases keeps secretions fluid and the endotracheal tube patent. A high oxygen concentration compensates for deficient oxygen uptake and transport caused by pulmonary lesions and the presence of poisonous compounds interfering with oxygen transport. Dexamethasone to minimise cerebral oedema and antibiotics to reduce the incidence of chest infections should be given.     

Reactive oxygen species: influence on cerebral vascular tone.

Reactive oxygen species have multiple effects on vascular cells. Defining the sources and the impact of the various reactive oxygen species within the vessel wall has emerged as a major area of study in vascular biology. This review will focus on recent findings related to effects of reactive oxygen species on cerebral vascular tone. Effects of superoxide radical, hydrogen peroxide, and the reactive nitrogen species peroxynitrite are summarized. Although higher concentrations may be important for cerebral vascular biology in disease, relatively low concentrations of reactive oxygen species may function as signaling molecules involved with normal regulation of cerebral vascular tone. The mechanisms by which reactive oxygen species affect vascular tone may be quite complex, and our understanding of these processes is increasing. Additionally, the role of reactive oxygen species as mediators of endothelium-dependent relaxation is addressed. Finally, the consequences of the molecular interactions of superoxide with nitric oxide and arachidonic acid are discussed.     

Advances in the Understanding and Treatment of Head Injury

The author describes his personal involvement in head injury prevention and management over the past 40 years. He reviews the evolution of knowledge concerning the role of increased intracranial pressure, and considers the importance of cerebral vasoparalysis in the production of signs and symptoms following head injury, and the development of methods of recording intracranial pressure continuously, over hours and days.The development of an experimental compression model has led to a fuller understanding of edema of the brain and has provided a means of studying, by light and electron microscopy, the histological changes that result from edema. More recently, analyses of biochemical changes and disturbed membrane function have opened up a new avenue of potential treatment. Moreover, it is now clear that cerebral vascular dilatation and abrupt pressure increase can be produced in the monkey, in over 50% of cases, by lesions in the dorsomedial nucleus of the hypothalamus. Similar lesions may occur in the human and this suggests other therapeutic approaches. There is, then, a genuine hope of a breakthrough in the management of head injuries.     

ELBOW AND WRIST INJURIES IN SPORTS

Any disabling injury of the elbow or wrist should be studied roentgenographically for evidence of fracture which may not be otherwise evident but which may cause permanent disability unless the joint is immobilized for healing.“Tennis elbow” may be treated with physical therapy and analgesic injection but may require splinting or tendon stripping. Elbow sprain can occur in the growing epiphysis but is rare in adults. A jarring fall on the hand may cause fracture or dislocation at the elbow.Full extension of the joint should be restored gradually by active exercise rather than passive or forcible stretching.Fracture at the head of the radius may cause joint hemorrhage with severe pain which can be relieved by aspiration. A displacing fracture at the head of the radius requires removal of the head to prevent arthritic changes. Myositis ossificans contraindicates operation until after it has cleared.Healing of wrist fractures may be facilitated by exercise of the shoulder and elbow while the wrist is still in a cast. Fractures of the navicular bone are difficult to detect even roentgenographically and splinting may have to be done on clinical evidence alone.     

THE EFFECT OF IONIZING RADIATION UPON MITOCHONDRIA OF THE CENTRAL NERVOUS SYSTEM

After irradiation of rats with a linear electron accelerator, the respiratory rate in rat brain mitochondria was studied in the presence of substrate + ADP and after the conversion of ADP → ATP. After 20,000 rads of irradiation to the head there was a transient diminution of mitochondrial respiratory control when glutamate was used as the substrate, but no changes were observed when succinate was the substrate. Irradiation with 10,000 rads had no effect upon respiratory control. The addition of NADH₂ to irradiated mitochondria had no effect upon mitochondrial respiration. Irradiation of the brain with 20,000 rads failed to produce mitochondrial peroxidation or swelling, even in the presence of FeNH₄(SO₄)₂ or ascorbate. The slight changes in respiratory control of brain mitochondria following irradiation is in marked contrast to the susceptibility of mitochondria from other organs. The comparative radioresistance of brain mitochondria may be the result of greatly diminished radiation-induced peroxidation of cerebral mitochondrial membranes.     

JNK3 signaling pathway activates ceramide synthase leading to mitochondrial dysfunction

A cardinal feature of brain tissue injury in stroke is mitochondrial dysfunction leading to cell death, yet remarkably little is known about the mechanisms underlying mitochondrial injury in cerebral ischemia/reperfusion (IR). Ceramide, a naturally occurring membrane sphingolipid, functions as an important second messenger in apoptosis signaling and is generated by de novo synthesis, sphingomyelin hydrolysis, or recycling of sphingolipids. In this study, cerebral IR-induced ceramide elevation resulted from ceramide biosynthesis rather than from hydrolysis of sphingomyelin. Investigation of intracellular sites of ceramide accumulation revealed the elevation of ceramide in mitochondria because of activation of mitochondrial ceramide synthase via post-translational mechanisms. Furthermore, ceramide accumulation appears to cause mitochondrial respiratory chain damage that could be mimicked by exogenously added natural ceramide to mitochondria. The effect of ceramide on mitochondria was somewhat specific; dihydroceramide, a structure closely related to ceramide, did not inflict damage. Stimulation of ceramide biosynthesis seems to be under control of JNK3 signaling: IR-induced ceramide generation and respiratory chain damage was abolished in mitochondria of JNK3-deficient mice, which exhibited reduced infarct volume after IR. These studies suggest that the hallmark of mitochondrial injury in cerebral IR, respiratory chain dysfunction, is caused by the accumulation of ceramide via stimulation of ceramide synthase activity in mitochondria, and that JNK3 has a pivotal role in regulation of ceramide biosynthesis in cerebral IR.     

Management of Cardiac Arrest: A Discussion of Cardiorespiratory Resuscitation

In cases of sudden cardiac arrest the time limit during which anoxic brain damage can be reversed is about four minutes. Therefore, cardiorespiratory resuscitation must be instituted immediately. A simple plan requiring no complicated maneuvers or equipment should be memorized and employed in such cases. The following program is recommended: (1) Institute artificial ventilation. (2) Thump the chest once or twice. (3) Employ closed chest compression. (4) Transfer the patient to hospital if survival appears possible. (5) Obtain an electrocardiogram immediately. (6) Apply specific treatment for cardiac standstill or ventricular fibrillation. (7) Reassess after 30 minutes. Discontinue treatment if there has been no response; if the pupils have remained dilated, fixed and unresponsive to light for over 10 minutes; or if it has been ascertained that the patient has definite serious illness incompatible with continuing life. Such a plan as outlined above should be instituted at once, before attempting to determine the cause of cardiac arrest or planning further special treatment.