Showing papers on "Pain medicine published in 1979"

Chronic pain syndromes and their treatment. II. Trigger points.

Abstract: Trigger points are distinct areas of focal hyperirritability which give rise to areas of referred pain in well-defined areas of the musculoskeletal system, sometimes remote from the point itself and not related to it by anatomically definable pathways. While the vast majority of pain manifestations from trigger points are related to the musculo-skeletal system, this need not be invariably so, as has been demonstrated in two of the cases cited, where injection of trigger points in the neck relieved chronic tinnitus. In all manifestations of chronic pain it is recommended that a diligent search be made for such trigger points.

Pulmonary hypertension in the adult respiratory distress syndrome (ARDS)

Abstract: Activated charcoal hemoperfusion has been performed in 60 cases of acute poisoning. In a) deeply comatose patients (due to the effects of hypnotics and chlorinated solvents with high extracellular concentration) in order to reduce the duration of the coma b) those intoxications with a high mortality, such as Paraquat, Colchicine, Digitoxine, Tricyclic drugs and Heavy Metals, even when the blood levels were low compared to the ingested amount. This discrepancy can be related not only to a predominant intra-cellular binding, but also to poor intestinal absorption (as proved for Paraquat). The efficiency of Hemoperfusion has been estimated according to the amount of extracted drug measured

Monitoring the nutritional status of critically III patients

Abstract: The importance of adequate nutrition in the critically ill has been a subject of much recent interest [42]. With the development of systems of nutritional support using the enteral or parenteral route, it is now possible to meet the nutritional requirement of virtually all patients. However, definition of what is \"adequate\" is often very difficult. This results from the variable magnitude of the metabolic response to trauma or disease [ 10, 31 ], together with the specific problems associated with individual illnesses. In order to plan a nutritional regimen on a rational basis, it is necessary to have a quantitative estimate of the requirements for each of the main types of nutrients, namely energy substrates (carbohydrate and fat), amino acids (proteins), minerals and vitamins. Such an estimate will usually depend u p o n : (1) the existing nutritional state of the patient (2) daily consumption or utilisation of nutrients (3) the effect of provision of a particular level of nutritional support (4) the nature and severity of the illness or injury and the clinical management.

Acute renal failure due to rhabdomyolysis in sickle cell trait.

Abstract: We have studied the respiratory response to acute metabolic acidosis (AMA) in 159 patients with initial arterial pH values between 6.77 and 7.35. There is a curvilinear relationship between hydrogen ion concentration [H +] and arterial carbon dioxide tension as defined by Equation 1. It shows that the amplitude of the respiratory response decreases gradually as acidosis becomes more severe. The minimal value for PCO2 is observed for a pH around 6.90 and it increases for higher [H+]. The relationship between plasma [HCO3 ] and PCO2 is linear over a range of [HCO3 ] from 25 to 2 retool/1 (Equation 2). The same is true for the relationship between base excess and PCQ over a range from 2 to -25 retool/1 (Equation 3). The 95% significance bands for these two relationships are 8.5 and 10 mm Hg wide respectively. There is an important individual variation in the respiratory response to AMA, which is partly dependent on the age of the patient; the respiratory response to AMA decreases with age. Amongst patients who are repeatedly admitted to hospital for acute episodes of ketosis, it was possible to recognize a relative constancy in the response as shown by the same position in the significance band, suggesting individual difference in sensitivity to [H+]. The significance bands may be used to identify abnormal responses to AMA. Anxiety or pain are able to exacerbate hyperventilation. Chronic bronchopulmonary disease, sedatives, alcohol as well as extreme hypoor hyperkalemia tend to decrease the response and determine abnormally high PCO2 for a given pH. During and immediately after correction of acidosis with sodium bicarbonate, PCO2 value is maintained to a lower value than predicted. It is interesting to note that the respiratory response to AMA appears to be similar to that described in chronic metabolic acidosis among patients with chronic renal failure.

Nutritional status and body composition in critically Ill patients

Abstract: Pulmonary hypertension in ARDS therefore seems to be responsible for two hemodynamic abnormalities: 1) It imposes an elevated work load upon the right ventricle, which can produce right ventricular failure; continuous infusion of an inotropic agent helps to combat this. 2) It may be involved in systemic hypotension and abnormally low systemic arterial resistance that is present in ARDS (SAR: 24 + 9 UI for CI < 2 l/min/m 2, 19 + 5 UI for CI 2 3 1/min/m 2, 17 + 5 UI for CI 3 -4 1/min/m 2, 14 + 4 UI for CI > 4 1/min/m2).

Cardiac resuscitation services: principles and practice.

Abstract: \"Sudden death from heart attack is the most important medical emergency today\" [42]. The combination of the two basic manual techniques of cardiopulmonary resuscitation (CPR), expired air resuscitation and external cardiac massage, is barely twenty years old, but its widespread use has already saved countless lives in patients with \"hearts too good to die\" [3]. Accidental drowning is second only to road accidents as a cause of sudden death in healthy young people [38], whilst an acute ischemic heart attack [28] is the great killer in older persons, most untreated patients dying before they reach hospital [2]. But in both conditions cardiac arrest is reversible in up to half the cases with immediate CPR, emphasising the important role of public education in the use of \"basic life support\" techniques [42]. Moreover, the term \"unexpected\" can hardly be justified in the definition of cardiac arrest nowadays, when so many gravely ill patients in hospital are resuscitated, often successfully. Uncertain in time maybe, but hardly unexpected. The first aim of CPR is to protect the brain with manual techniques (Stage 1 of CPR), and it is here that swift action by the bystanders is vital, and delay lethal. Despite current, and promising, experimental and clinical work on its therapy [41], severe brain damage is inevitable if cerebral blood flow is interrupted for more than three to four minutes at normal body temperature, and delay in initiating resuscitation remains the dominant cause of brain damage from cardiac arrest. Efficient resuscitation usually protects the brain, even though its blood flow and hence its function is greatly impaired [ 19]. Heart action is restored within fifteen minutes in the majority of patients who leave hospital alive after cardiac arrest, \"long-term survivors\" [ 19]. Various factors play a role in this, and one of the most important is the functional state of the heart before it stops. It is much easier to restore and maintain satisfactory heart action when the myocardium is relatively healthy, and when cardiac arrest is precipitated by a sudden rhythm disturbance [28], \"electrical failure\" [21]. It is far more difficult when the myocardium is extensively and irreparably damaged, \"power failure\"J21]. Delay in initiating resuscitation also affects the results [1,12,31,34], since it not only damages the brain but the myocardium too. \"The balance between energy production and energy utilisation is precarious even in the normal myocardial cell\" [24] and its oxygen and energy stores are rapidly consumed when coronary blood flow ceases. Ventricular fibrillation, by far the commonest dysrhythmia at the moment of cardiac arrest in adults, [1,37] can accelerate exhaustion of these stores when the heart is diseased [23]. If resuscitation is delayed more than a few minutes, resistant asystole will succeed ventricular fibrillation and the patient is now unlikely to survive [1,15,34,46], for the myocardium is now irreversibly damaged and its cells cannot even generate an electrical signal. Even if heart action is restored, the patient now has a reduced chance of survival [ 14], whereas prompt resuscitation protects the heart. The importance of these various factors is greatly enhanced where the myocardium is in jeopardy even before cardiac arrest, as in ischemic heart disease, for here delay in resuscitation may ensure the death of threatened myocardium and convert electrical failure into power failure. Protracted resuscitation too may be harmful. Ventricular fibrillation interferes with myocardial, and especially subendocardial blood flow, [5,22], and this is aggravated by the low cardiac output and associated low diastolic blood pressure of CPR. Moreover, CPR is often, and in some respects inevitably accompanied by progressive pathophysiological changes [19,36] such as lactic acidosis, hypoxemia, and after major trauma hyperkalemia, and these too can depress the heart and also the brain. But whilst the brain will afterwards gradually recover completely from the ill-effects of protracted resuscitation, the heart must swifty regain satisfactory function whenits actionis restored if the patient is to survive. A good circulation is also vital to the recovery of a brain damaged by delayed resuscitation [18]. It is clear that the best moment for the restoration of heart action is immediately after the onset of cardiac arrest, before these various harmful changes have had time to develop. Immediate countershock for ventricular fibrillation has rightly become the first step in resuscitation in special care Units, and its \"blind\" use is fully justified

Plasma exchange in the treatment of myasthenia gravis.

Abstract: In the past year we have treated 15 patients with Myasthenia Gravis (M.G.) by Plasma Exchange (P.E.). The age of onset of the M.G. ranged from 14 to 69 years, and the disease had been present from 6 months to 23 years. The clinical severity as measured by the Ossermann scale was grade II A in 1 patient, II B in 4 patients, III in 4 patients and IV in 6 patients. 10 patients were thymectomized (5 had thymoma). The previous treatment consisted of either anticholinesterase drugs alone (11 patients) or was associated with corticosteroids for at least 1 month (3 patients). The plasma volume exchange during each continuous flow P.E. was of 5 liters and was replaced with 50% plasma substitutes and 50% purified human albumin, 10 g of human gammaglobulins were given intravenously after each set. 3 P.E. were performed in one week. 2 or 3 additional exchanges were decided upon from the clinical findings. Additional treatment consisted of anticholinesterasic drugs and corticosteroids (1 mg/Kg/day) in 12 patients. Azathioprine was added in one patient. 2 patients received anticholinesterasic drugs only. During the P.E. 3 patients had rigors with fever and hypotension, 1 had acute hypovolemia, and 2 had secondary hypercoagulation requiring heparin treatment; 10 patients were improved after 2 or 3 P.E. and before corticosteroid treatment, Vital capacity improvement by 11% to 30%, in 4 patients with parallel improvement of swallowing; Vital capacity remained stable in 2 cases but with improved muscular and oro pharyngeal strength; 4 patients with initially normal capacity fully recovered after 2 P.E.; 3 patients did not improve after 4 P.E. in 10 days with very gradual subsequent improvement by corticosteroids; 2 patients initially improved but relapsed 2 to 5 months later, with no effect on renewed P.E. We conclude that P.E. is active in most cases. Because the effect is transitory. P.E. seems best indicated to prevent the clinical deterioration of M.G. that occurs at the onset of corticosteroid therapy. Patients resisting P.E. cannot be further assessed without determination of Ach. R. antibodies. Secondary resistance may be due to a rebound phenomenon with irreversible binding of Ach. R. antibodies.