Jerome P. Kassirer

A convenient approximation of life expectancy (the “DEALE”): II. Use in medical decision-making☆

We show how to use a bedside approximation of life expectancy in quantitative decision-making. This method, the declining exponential approximation of life expectancy (DEALE), enables the physician to collate various survival data with information on morbidity to determine a quality-adjusted expected survival for a potential management plan. The keystone in the DEALE approach is the approximation of survival by a simple exponential function. This approximation makes it possible to translate data from various literature sources (life expectancy tables, five-year survival rates, survival curves, median survival) into a single, unified mortality scale. In this paper, we use the DEALE method to obtain approximations of quality-adjusted life expectancy and illustrate the application of the method in a quantitative analysis of a clinical decision.

Our stubborn quest for diagnostic certainty. A cause of excessive testing.

Absolute certainty in diagnosis is unattainable, no matter how much information we gather, how many observations we make, or how many tests we perform. A diagnosis is a hypothesis about the nature ...

Decision Analysis: A Progress Report

Since its introduction into medicine 15 years ago, decision analysis has been applied to difficult clinical problems. Several important advances have made the process more practical and acceptable: computer programs that eliminate the need for burdensome calculations, improved techniques for designing analytic models, the ability to carry out sensitivity analyses over several dimensions simultaneously, and the elaboration of clinically relevant measures of utility. Using these techniques, analysts have addressed many important clinical issues including screening for and prevention of disease, tradeoffs among tests and treatments, and the interpretation of clinical data under conditions of uncertainty. Problems with the approach remain and applications have not been extensive, but decision analysis is evolving as a powerful clinical tool and gradually is gaining acceptance in medical practice.

Decision analysis and clinical judgment

Abstract Sound clinical judgments derive both from the command of a sufficient body of facts and from the skill to combine such facts appropriately. Most undergraduate and graduate medical education concentrates on the first of these elements, the acquisition of knowledge; little formal effort is directed to the logic of dealing with clinical problems. In this discussion we suggest that the theory and technics of decision analysis provide new and useful strategies appropriate for dealing with complex clinical situations. In their qualitative aspects these formal strategies closely resemble those that the expert clinician employs informally, but which he is often unable to communicate explicitly. When applied quantitatively, the formalism affords greater precision than is otherwise readily attainable. To illustrate the application and utility of decision analysis we have considered the problems posed by severely hypertensive patients with possible functional renal artery stenosis, and have examined, both qualitatively and quantitatively, the alternative courses of action available to the clinician.

Causal reasoning in medicine: Analysis of a protocol

The ability to identify and represent the knowledge that a human expert has about a particular domain is a key method in the creation of an expert computer system. The first part of this paper demonstrates a methodology for collecting and analyzing observations of experts at work, in order to find the conceptual framework used for the particular domain. The second part develops a representation for qualitative knowledge of the structure and behavior of a mechanism. The qualitative simulation, or envisionment, process is given a qualitative structural description of a mechanism and some initialization information, and produces a detailed description of the mechanisms behavior. The simulation process has been fully implemented, and its results are shown for a particular disease mechanisms in nephrology. This vertical slice of the construction of a cognitive model demonstrates an effective knowledge acquisition method for the purpose of determining the structure of the representation itself, not simply the content of the knowledge to be encoded in that representation. Most importantly, it demonstrates the interaction among constraints derived from the textbook knowledge of the domain, from observations of the human expert, and from the computational requirements of successful performance.

Losing Weight — An Ill-Fated New Year's Resolution

Today, at the start of the new year, millions of Americans will resolve to lose weight, but by tomorrow, or next week, or maybe next month, most of them will have given up trying. Few will have los...

Managed Care and the Morality of the Marketplace

Whether health care should be subjected to the values of the marketplace is a fundamental question facing us today. A powerful trend in this direction is upon us, with enormous, well-financed compa...

Cognitive errors in diagnosis: Instantiation, classification, and consequences

To identify diagnostic errors caused by faulty clinical cognition, we analyzed 40 consecutive transcripts of problem-solving exercises published in a pedagogic series of clinical reasoning. The analysis disclosed multiple errors in cognition and produced a provisional classification of these errors based on a framework derived from cognitive science. Faults in cognition were identified in all steps of the diagnostic process, including triggering, context formulation, information gathering and processing, and verification. We instantiated each type of error by providing detailed specific examples, and identified the consequences of each error. We conclude that cognitive errors can be identified and classified, that they can produce serious morbidity, and that a classification of cognitive errors is a step toward a deeper understanding of the epidemiology, causes, and prevention of diagnostic errors.

The response of normal man to selective depletion of hydrochloric acid: Factors in the genesis of persistent gastric alkalosis☆

Abstract Factors responsible for the development of gastric alkalosis in man have been examined by means of selective depletion of hydrochloric acid without concomitant extrarenal depletion of sodium, potassium or water. Throughout the study the subjects ingested a diet of normal composition except for its low sodium and chloride content. In each instance the removal of hydrochloric acid led to the development of persistent metabolic alkalosis (plasma bicarbonate concentration 34 to 39, mEq. per L.), and augmented renal potassium excretion. There was little or no change in sodium balance. The constancy of the glomerular filtration rate and of serum sodium concentration indicate not only that the renal threshold for bicarbonate was elevated but also that the rate of sodium-hydrogen exchange was accelerated. The data demonstrate that an extrarenal loss of sodium, potassium and water during vomiting or gastric drainage in man is not a prerequisite to the development of sustained metabolic alkalosis or potassium deficiency. It is evident that the observed cation and water deficits develop as the result of secondary renal adjustments to hypochloremia. The characteristics of a mechanism which appears to account for these renal adjustments have been considered.

The critical role of chloride in the correction of hypokalemic alkalosis in man

Abstract Studies of hypokalemic metabolic alkalosis in man have demonstrated that the provision of chloride is a prerequisite to restoration of normal acid-base and potassium equilibrium. In both experimentally-induced and diuretic-induced alkalosis the ingestion of a liberal quantity of dietary potassium had no effect on plasma bicarbonate concentration if chloride intake was simultaneously restricted. Furthermore, the administration of a dietary supplement of potassium in the form of bicarbonate or neutral phosphate also failed to correct the acid-base disturbance. Although potassium balance was slightly positive during loading with potassium bicarbonate or neutral phosphate, full repletion of body potassium stores could not be effected on the low chloride diet. By contrast, the administration of chloride as either the sodium or potassium salt led to a suppression of acid excretion with a prompt return of plasma bicarbonate concentration to normal; there was a simultaneous striking retention of potassium, and restoration of a normal serum potassium concentration. On the basis of these findings, and of earlier experimental observations in the dog, it has been proposed that so long as hypochloremia persists, a disproportion between the quantity of sodium reabsorbed and the amount of penetrating anion available for reabsorption (i.e., chloride) will maintain an accelerated rate of sodium-hydrogen and sodium-potassium exchange. This acceleration of the exchange process sustains both a high renal threshold for bicarbonate and prevents full repair of the potassium deficit. Only when chloride is made available can the accelerated rate of cation exchange be restored to normal. The possible implications of these findings in the treatment of hypokalemic alkalosis as it occurs in a variety of clinical settings are considered.