John B. Dossetor

Syndrome associated with the abuse of analgesics.

Abstract Twenty-two patients with renal disease seen over a 4-year period had abused analgesics containing acetylsalicylic acid, phenacetin, caffeine, and in all but one instance codeine. The minim...

THE SIGNIFICANCE OF LACTICACIDEMIA IN THE SHOCK SYNDROME

William Cannon as long ago as 1918 noted a rough correlation between “the severity or duration of hypotension and the decrease in carbon dioxide combining power of the blood.” He wrote: “There is a relationship between blood flow, and hence tissue perfusion and blood p H values.” Tissue underperfusion may result from decreased perfusing pressure or increase in vasoconstriction. The term “shock” has generally been retained to describe a multietiological syndrome characterized by hypotension, tachycardia, cold moist extremities, and pallor. The degree of shock traditionally is judged by the level of systemic arterial pressure. However, it is likely that the basic problem in shock is “an inadequate flow of blood into the capillary beds of skin and other organs” (Simeone, 1960). Thus, a measurement that quantitates the extent to which tissues are inadequately perfused should give a more accurate index of severity than can blood pressure, which is dependent upon both peripheral vascular resistance and cardiac output. Inadequate perfusion of tissues results in partial arrest of glycolysis a t the anaerobic phase, with accumulation of lactate and other ions as a consequence of the decreased tissue pop (FIGURE 1). Lactate, the predominant ion in this system, is readily diffusible. Therefore, the degree of underperfusion can be assessed by measurement of the concentration of lactate in the blood. Cournand and his collaborators (1943) showed that an uncompensated metabolic acidosis develops with many different forms of shock, and their data indicate that there is a rough correlation between the degree of acidosis and the severity of the shock as judged by arterial blood pressure. Subsequently, Cruz and his co-workers (1954) demonstrated in dogs that shock induced with antiplatelet serum showed a direct correlation between severity, as judged by survival rate, and the degree of accumulation of arterial blood lactate. Crowell (1960) and Crowell and Guyton (1961 & 1962) reported a 100 per cent survival rate in those dogs subjected to hemorrhagic shock, with an oxygen debt of up to 100 ml. of oxygen per kg., in which the blood was retransfused and the arterial pressure brought back to normotensive levels before the oxygen debt had exceeded this limit. However, none survived an accumulation

Aseptic Necrosis Following Renal Transplantation

In twenty-seven patients who survived for six months or longer following renal homotransplantation, osseous changes developed in ten patients. Nine demonstrated aseptic necrosis of the femoral head, five had involvement of the hips alone, five showed aseptic necrosis at the knee joint, and two had aseptic necrosis of the humeral heads. The average time after transplantation when symptoms arose was seven months and the roentgen changes usually were seen two months later. The etiological explanation based on fatty embolization is theoretically satisfactory but unproved.

Essential Hypertension and Aldosterone

Serial determinations of the urinary excretion of aldosterone have been made in hypertensive patients. Although the majority of patients with benign essential hypertension excrete amounts of aldosterone within the normal range, the mean excretion of 26 patients was significantly higher than that observed in normotensive individuals. When renal complications were present, the mean excretion was still further increased and in patients with malignant hypertension all the values were above the normal range. The mean excretion of the tetrahydro metabolite of aldosterone was also found to be higher in patients with essential hypertension. These patients have a normal response to adrenocorticotrophic hormone stimulation, urinary and plasma corticosteroids, as well as urinary aldosterone, showing comparable increases. The aldosterone content of adrenal glands obtained post mortem from two patients with malignant hypertension was within the range observed by other investigators in primary aldosteronism.

Hyperchloremic Acidosis in Early Diagnosis of Renal Allograft Rejection

Abstract Hyperchloremic renal tubular acidosis has been observed to occur in a surprisingly high percentage of episodes of rejection in patients who have had cadaver renal allografts. Impairment of...

HYPERLACTATEMIA DUE TO HYPERVENTILATION: USE OF CO2 INHALATION

Two cases will be presented in which hyperlactatemia occurred without acidosis and the degree of lactatemia decreased significantly when CO, was administered as therapy. H~ckabee , ’ .~ Eichenholz and collaborators,‘ and others’ have shown that lactatemia occurs with hyperventilation, both in man and in dogs. Huckabee states that this is a form of lactatemia in which “excess lactate” does not occur, i.e., the lactate/pyruvate ratio would remain normal. I t is inferred that the condition in man is usually benign and passes off when the cause of hyperventilation is controlled. We would not disagree with the latter part of this statement but have evidence that the benign nature of these states leaves something to be desired. Whether this form of lactatemia should be considered as “a compensatory mechanism” or not is a matter of opinion. Eichenholz et al.‘ have shown that the primary respiratory alkalosis may lead, through secondary lactatemia, to an eventual acidosis. This suggests that the mechanism is not truly compensatory. Primary hyperventilation giving rise to an initial respiratory alkalosis occurs in man in a number of diseased states: (1) voluntary or hysterical hyperventilation; (2) CNS lesions, e.g., cerebrovascular accidents; (3) anoxemia, especially a t altitude6 and possibly also in pneumonic stiffness of lung (in these instances the lactatemia may be partly due to the effects of anoxemia as well as hyperventilation, i.e., mixed cases); (4 ) hepatic coma;’ (5) salicylate poisoning; and (6) excessive ventilation by artificial means on a respirator or under anesthesia. We believe that acute Wernicke’s encephalopathy (as will be described in one of the patients below) may also be associated with a pathological disorder of acid base homeostasis on the basis of hyperventilation. Eichenholz‘ has emphasized an important facet of lactatemia that occurs with primary hyperventilation, namely, that if five per cent CO, in air or oxygen is used as the respiratory gas, hyperlactatemia is prevented and will not occur despite continuation of hyperventilation. Further, if the gas mixture is changed from air to the Con mixture after hyperlactatemia has been induced by either salicylate or passive hyperventilation, the level of lactate will fall and the serum bicarbonate concentration will rise, concomitantly. The fact that several observers have noticed that hyperlactatemia occurs with hyperventilation of the passive type refutes the theory that this mechanism is due to the work involved in hyperventilation itself.