Bacterial disease caused by a toxin produced by the bacterium Staphylococcus aureus. It was first recognized in 1978 in women using superabsorbent tampons. High fever, diarrhea, vomiting, and rash may progress to abdominal tenderness, drop in blood pressure, shock, respiratory distress, and kidney failure. The syndrome also has other causes, including postsurgical infection. Antibiotics are not effective. With intensive supportive therapy, most patients recover in 7–10 days, but 10–15percnt die. Many patients have a milder recurrence within eight months.
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Device for controlling unwanted motion of a spring-mounted vehicle. On an automobile, the springs act as a cushion between the axles and the body and reduce the shocks produced by a rough road surface. Since some combinations of road surface and car speed may result in excessive up-and-down motion of the car body, shock absorbers—which today are hydraulic devices that oppose both compression and stretching of the springs—slow down and reduce the magnitude of these vibratory motions. Seealso damping.
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State in which the circulatory system fails to supply enough blood to peripheral tissues to meet basic requirements. Symptoms—weak, rapid pulse; low blood pressure; and cold, sweaty skin—are not all present in every case. Causes include low blood volume, caused by bleeding or fluid loss from burns or dehydration; inability of the heart to pump enough blood, due to heart attack, pulmonary embolism, or cardiac tamponade (compression of the heart by fluid in the membrane around it); and blood-vessel dilation as a result of septicemia, allergy (including anaphylaxis), or drugs. All result in reduced capillary blood flow; reflexes increase heart rate and constrict small blood vessels to protect the blood supply to essential organs. Without treatment of the underlying cause, these mechanisms fail; since the cause is not always clear, cases tend to require different and occasionally contradictory treatment (e.g., intravenous fluids can save the life of a patient with massive blood loss but can overload a weakened heart).
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Physical effect of an electric current that enters the body, ranging from a minor static-electricity discharge to a power-line accident or lightning strike but most often resulting from house current. The effects depend on the current (not the voltage), and the worst damage occurs along its path from the entry to the exit point. Causes of immediate death are ventricular fibrillation and paralysis of the brain's breathing centre or of the heart. Cardiopulmonary resuscitation is the best first aid. Though most survivors recover completely, aftereffects may include cataract, angina pectoris, or nervous-system disorders.
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Circulatory shock, commonly known as just shock, is a serious, life-threatening medical condition where insufficient blood flow reaches the body tissues. As the blood carries oxygen and nutrients around the body, reduced flow hinders the delivery of these components to the tissues, and can stop the tissues from functioning properly. The process of blood entering the tissues is called perfusion, so when perfusion is not occurring properly this is called a hypoperfusional (hypo = below) state.
Circulatory shock should not be confused with the emotional state of shock, as the two are not related. Medical shock is a life-threatening medical emergency and one of the most common causes of death for critically-ill people. Shock can have a variety of effects, all with similar outcomes, but all relate to a problem with the body's circulatory system. For example, shock may lead to hypoxemia (a lack of oxygen in arterial blood) or cardiac arrest (the heart stopping).
There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next. Initial : During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate (ATP). Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extra-cellular fluid, and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent. Compensatory (Compensating) : This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline. Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin-angiotensin axis is activated and arginine vasopressin is released to conserve fluid via the kidneys. Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin-angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock. Progressive (Decompensating) : Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting the increased complication of endotoxic shock. Refractory (Irreversible): At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death have occurred. Death will occur imminently.
Recently a fifth form of shock has been introduced:
In the early stages, shock requires immediate intervention to preserve life. Therefore, the early recognition and treatment depends on the transfer to a hospital.
The management of shock requires immediate intervention, even before a diagnosis is made. Re-establishing perfusion to the organs is the primary goal through restoring and maintaining the blood circulating volume ensuring oxygenation and blood pressure are adequate, achieving and maintaining effective cardiac function, and preventing complications. Patients attending with the symptoms of shock will have, regardless of the type of shock, their airway managed and oxygen therapy initiated. In case of respiratory insufficiency (i.e. diminished levels of consciousness, hyperventilation due to acid-base disturbances or pneumonia) intubation and mechanical ventilation may be necessary. A paramedic may intubate in emergencies outside the hospital, whereas a patient with respiratory insufficiency in-hospital will be intubated usually by a respiratory therapist, paramedic, or physician.
The aim of these acts is to ensure survival during the transportation to the hospital; they do not cure the cause of the shock. Specific treatment depends on the cause.
A compromise must be found between:
This is the stay and play versus the load and go debate.
Regardless of the cause, the restoration of the circulating volume is priority. As soon as the airway is maintained and oxygen administered the next step is to commence replacement of fluids via the intravenous route.
Opinion varies on the type of fluid used in shock. The most common are:
It is to be noted that NO plain water should be given to the patient at any point, as the patient's low electrolyte levels would easily cause water intoxication, leading to premature death. An isotonic or solution high in electrolytes should be administered if intravenous delivery of recommended fluids is unavailable.
Vasoconstrictor agents have no role in the initial treatment of hemorrhagic shock, due to their relative inefficacy in the setting of acidosis, and because the body, in the setting of hemorrhagic shock, is in an endogenously catecholaminergic state. Definitive care and control of the hemorrhage is absolutely necessary, and should not be delayed.
The main goals of the treatment of cardiogenic shock are the re-establishment of circulation to the myocardium, minimising heart muscle damage and improving the heart's effectiveness as a pump. This is most often performed by percutaneous coronary intervention and insertion of a stent in the culprit coronary lesion or sometimes by cardiac bypass.
Although this is a protection reaction, the shock itself will induce problems; the circulatory system being less efficient, the body gets "exhausted" and finally, the blood circulation and the breathing slow down and finally stop (cardiac arrest). The main way to avoid this deadly consequence is to make the blood pressure rise again with
Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction of the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood in reinfused. In pigs and humans 1) this is not seen and cessation of bleeding and restoration of blood volume is usually very effective; however 2) prolonged hypovolemia and hypotension does carry a risk of respiratory and then cardiac arrest. Perfusion of the brain may be the greatest danger during shock. Therefore urgent treatment (cessation of bleeding, rapid restoration of circulating blood volume and ready respiratory support) is essential for a good prognosis in hypovolemic shock.