~~,odia~,i,-A,,ociasd AypotBndion

w,I"piam 1 A e n r U X , Serie, C d ; & P

Factors Which Affect Cardiac Performance during Hemodialysis

Mark Travis and William L. Henrich

From the Departments of Internal Medicine and Nephrology, University of Texas Southwestern Medical School and Dallas Veterans Administration Medical Center, Dallas, Texas

Cardiovascular disease remains the leading cause of morbidity and mortality in patients undergoing chronic hemodialysis. In most circumstances, is- chemic cardiomyopathy is the primary form of heart disease affecting dialysis patients. The etiology of atherosclerosis in patients with end-stage renal dis- ease (ESRD) is multifactorial; antecedent hyperten- sion and lipid abnormalities which accompany kid- ney failure are of obvious importance in the gener- ation of disease. Several studies have sought to determine whether or not the chronic dialysis pro- cedure itself actually accelerates the atherosclerotic process, but the results have been conflicting (1-4). The problem with investigating this issue is that adequately controlling for predialysis coronary risk factors in a heterogeneous population of dialysis patients is difficult at best. Sufiice it to say that most investigators now agree that premorbid coronary risk factors (hypertension, advanced age, race, high cho- lesterol, and gender) are certainly important in the progression of atheromata (5).

Underlying coronary disease in the hernodialysis population is often uncovered because the dialysis procedure may be hemodynamically stressfbl. In fact, cardiac performance and its response to this stress dictates the overall success of dialysis. The hemodynamic response to hernodialysis is due to a complex interplay of factors: the autonomic nervous system, myocardial reserve (both inotropic and chronotropic), changes in volume status, plasma os- molality changes, dialysate constituents such as cal- cium and potassium, and pencardial disease.

This brief review examines several determinants of cardiac performance relevant to the hernodialysis procedures. A discussion of normal hemodynamics is followed by discussions of the hernodialysis pro- cedure in acute and chronic renal failure.

Address correspondence to: William L. Henrich, MD. Uni- versity of Texas Southwestern Medical Center-Dallas, Chief. Nephrology Service (1 1 IG I ) , Dallas VA Medical Center. 4500 S. Lancaster Rood, Dallas, TX 75216.

Seminars in Dialysis-Vol2, No 4 (Oct-Dec) 1989 pp 241- 245

Normal Ventricular Function

The stroke volume of the heart depends upon the initial stretch of the myocardial muscle (preload), intrinsic myocardial contractility (actin-myosin cou- pling), and the opposing force that myocardial mus- cular contraction must move against (afterload). Car- diac output is the product of the stroke volume and heart rate. Starling has emphasized that there is a relationship between cardiac output and left ventric- ular end diastolic pressure and volume. During dia- stolic filling of the left ventricle, myocardial compli- ance is defined by the curvilinear left ventricular pressure-volume relationship (LVEDV/LVEDP). By this relationship it is apparent that, at a given point in diastole, a small increase in LVEDV may sharply increase LVEDP. In simpler terms, the ventricle becomes less compliant with progressive filling.

Changes in plasma volume may markedly alter left ventricular end diastolic dimension and func- tion. For example, an increase in plasma volume typically increases diastolic myocardial fiber disten- tion and subsequently increases the quantity and the rate of ejection of stroke volume. In contrast, a reduction in plasma volume reduces myocardial stretch and lowers the stroke volume. Myocardial hypertrophy, a common pathologic finding in pa- tients with ESRD, reduces ventricular compliance. Thus, rapid volume expansion, particularly in the presence of a hypertrophied noncompliant ventricle, can increase LVEDP disproportionately to LVEDV and create pulmonary vascular congestion. For this reason, patients with LV hypertrophy on dialysis are not only prone to hypotension but are also suscep tible to volume overload and pulmonary edema. In short, many patients with ESRD operate within a narrower left ventricular volume/pressure relation- ship which makes adjustments to sudden volume changes more tenuous.

Afterload is defined as the wall tension needed to generate pressure sufficient to exceed aortic diastolic pressure within the cardiac chambers. Changes in plasma volume and myocardial hypertrophy a&ct afterload relationships by altering ventricular dimen-

24 1

242 Travis and Henrich

sions. Unfortunately, direct measurements of intrin- sic myocardial contractility are not available, and thus are estimated in the majority of cases. Table 1 lists the hemodynamic indices commonly utilized to describe ventricular function.

Hemodynamics in Renal Failure Syndromes

Acute Renal Failure

The predominant cardiac abnormalities in acute renal failure are typically due to plasma volume expansion. Defazio et al. (6) originally described a group of seven patients with acute oliguric glomer- ulonephritis who clinically manifested hypertension, peripheral edema, gallop rhythms, and pulmonary congestion. The hemodynamic perturbations noted were an increased cardiac output, stroke volume, right ventricular filling pressure, and a normal total peripheral vascular resistance. Overt myocardial dys- function was excluded in this study by a normal circulation time. The authors concluded that hyper- volemia secondary to the oliguric renal failure best explained these hemodynamic findings.

Agrest and Finkielman (7) observed similar car- diac hemodynamic parameters in volume over- loaded patients with acute renal failure caused by acute tubular necrosis. A subset of patients with acute renal failure had a different hemodynamic profile: these patients had an increased cardiac index, heart rate, and mean arterial pressure. However, total peripheral resistance was low and, importantly, blood volume was normal. These patients demon- strated a hyperdynamic circulation similar in many respects to other high cardiac output states such as hyperthyroidism. anemia, Paget’s disease, beriberi, and pregnancy. These authors speculated that the hyperkinetic circulation was a primary circulatory derangement and suggested that elevated levels of angiotensin caused a vasoregulatory defect. Thus, at least two hemodynamic patterns have been noted in patients with acute renal failure without underlying myocardial dysfunction. The pattern observed de-

TABLE 1. Hernodynamic indices describing ventricular performance

Preload parameters Central venous pressures Pulmonary capillary wedge pressure Left ventricular end-diastolic volume/dimension Total blood volume

Intrinsic myocardial contractility parameters Myocardial systolic shortening fraction Mean velocity of circumferential myocardial fiber shortening dP/dt Systolic time intervals Ratio of wall thickness of chamber ratios in relationship to

ventricular systolic pressure Afterload parameters

Left ventricular end-diastolic pressure Total peripheral vascular resistance

Ejection fraction Stroke volume and stroke index Cardiac output and cardiac index

Overall myocardial performance parameters

pended upon the plasma volume status accompa- nying the renal failure.

Chronic Renal Failure

Several hemodynamic investigations in patients with chronic renal failure (8-14) have shown an increased cardiac index, heart rate, peripheral vgs- cular resistance, and mean arterial pressure. Some investigators have noted a normal cardiac output ( 14) but methodological differences (e.g., different cardiac output techniques, sampling errors) have made comparisons difficult. The stroke index of chronic renal failure patients is usually described as normal or increased. A multiplicity of factors con- tribute to this hemodynamic profile: anemia, in- creased activity of the renin-angiotensin system, in- creased catecholamine concentrations, and ex- panded extracellular fluid (ECF) volume are just a few.

Goss et al. ( 1 5) suggested that the increase in blood pressure and cardiac output observed in chronic renal failure were directly related to sodium and water retention. In support of this hypothesis, Goss et al. (1 5) noted that either ultrafiltration dialysis or ultrafiltration alone was effective in blood pressure control since both remove sodium and water. How- ever, in a minority of ESRD patients with hyperten- sion, volume depletion does not control blood pres- sure. When compared to the volume-responsive hy- pertensive patients, these patients have a lower cardiac output and a higher peripheral vascular re- sistance. Plasma renin activity, aldosterone, and an- giotensin levels are also increased in this latter group, suggesting that these vasoregulatory substances are related to the increased peripheral resistance and blood pressure.

Kim et d. (1 1) observed that total peripheral vas- cular resistance was elevated only in hypertensive patients with renal failure. In these patients, bilateral nephrectomy resulted in a decrease in mean arterial pressure and total peripheral resistance which again suggested an important role for vasoregulatory sub- stances on peripheral vascular resistance. However, Rutsky and Rostand (16) pointed out that peripheral vascular resistance is always elevated when factored for the degree of anemia present in dialysis patients. These authors made hemodynamic observations in patients with chronic anemia (Hct 20%) which typ- ically showed an elevated cardiac index and a re- duced peripheral vascular resistance. Correction of anemia (Hct 30-3395) decreased cardiac index and increased peripheral vascular resistance. Neff et al. ( 10) further observed that when transfusions in- creased the hematocrit, a decrease in cardiac index and an increase in diastolic pressure and peripheral resistance occurred. Hence, it seems clear that differ- ences in the hemodynamic profile in patients with chronic renal disease is at least partially related to the degree of anemia. The recent availability of erythropoietin therapy and the resultant change in hematocnts in chronic dialysis patients may change

HD-WHAT AFFECTS CARDIAC PERFORMANCE? 243

the predominant hemodynamic patterns. Table 2 contrasts several hemodynamic profiles in patients with acute and chronic renal failure; patterns of hemodynamics in two dialysis procedures are also listed.

Hemodynamics of Hemodialysis

The hemodialysis procedure combines ultrafiltra- tion and diffusional solute clearance. Ultrafiltration is usually associated with a decrease in total blood volume, plasma volume, LVEDV, and stroke vol- ume. Therefore, in general, hemodialysis results in reduced left ventricular end-diastolic dimensions as a result of reduced central blood volume.

Variations in hemodynamic responses on hemo- dialysis occur depending on the rapidity of ultrafil- tration and the presence of myocardial dysfunction. Rapid mobilization of plasma volume, particularly with recently developed dialyzers with high ultrafil- tration coefficients, may produce hypotension. Di- alysis patients with diminished myocardial reserve would be expected to be prone to more frequent hypotension while on dialysis. Deleterious changes in LVEDV/LVEDP relationships, and diminished ability to augment intrinsic myocardial contractility could affect the cardiac response to volume loss. On the other hand, hemodialysis can actually improve myocardial performance. Gradual reductions in LVEDV (and LVED dimension) may improve myo- cardial performance by diminishing wall tension and afterload. Del Greco et al. (14) noted an increase in cardiac output concomitant with a decrease in pe- ripheral resistance after volume reduction in ESRD patients. Fernando et al. (17) and Chen and co- workers (18) also found an improvement in left ventricular function with hemodialysis.

Rouby et al. ( 19) investigated the individual effects of ultrafiltration and diffusional solute loss on the hemodynamic profiles of dialysis patients. Ultrafid- tration alone decreased LVEDP, pulmonary wedge pressure, and stroke volume, yet arterial pressure was stable and peripheral vascular resistance in- creased (20). When diffusional dialysis alone was performed, arterial pressure decreased and peripheral resistance failed to increase. When regular dialysis

(ultrafiltration and dialysis) was then performed, hy- potension occurred, despite a smaller amount of volume removal in comparison to ultrafiltration alone. The authors suggested that plasma osmolality, which was stable during isolated ultrafiltration, played a major role in the genesis of hypotension. They reasoned that d ih iona l dialysis reduced plasma osmolality and this impaired the expected hemodynamic response to volume depletion (21). Several investigators have subsequently documented the importance of a stable plasma osmolality for the maintenance of an adequate arterial pressure during dialysis. Therefore, hemodialysis may produce mul- tiple hemodynamic patterns depending on the amount and rapidity of volume removal, the pres- ence of prior myocardial dysfunction and dialysis procedural factors which affect osmolality and elec- trolytes.

Hfects of DialySat8 Calcium on Myocardial Performance during Hemodialysis. Several stud- ies have examined the importance of factors which might alter myocardial contractility directly during the dialysis procedure. Nixon et al. (22) noted an increase in the velocity of circumferential fiber short- ening (an index of contractility) after hemodialysis. This increase was independent of a volume change, and was latter shown to be associated with an in- creased ionized calcium concentration which occurs during dialysis (23). Kramer et al. (13) also noted an increased inotropic effect if the ionized calcium to potassium ratio was increased during the procedure, and Lang et al. (24) reported similar findings. In vitro experiments have shown that calcium facilitates the actin-myosin interaction and excitation coupling (25). Furthermore, calcium activates the ATPase necessary for the actin-myosin interaction.

Myocardial calcium content is increased in exper- imental uremia. It has been suggested that this may be the sequelae of myocardial cell death, subsequent fibrosis, hypertrophy or prolonged elevation of serum parathyroid hormone levels (26). Further, ouabain inhibition of sarcolemmal myocardial Na+/ Ca+ pump activity occurs in experimental models of uremia and this may partly explain the enhanced myocardial calcium burden. Whether increased myocardial calcium content is a result of the uremic

TABLE 2. Hernodynamic patterns in renal disease patients

Peripheral vascular

resistance Heart Stroke Cardiac Blood rate volume output pressure

~

Acute renal failure Patients with an increase in plasma volume -T T t T t Patients without an increase in plasma vol- T T r T 1

T t t T T

Volume responsive hypertensives T -T Volume unresponsive hypertensives t -T

V -1 T V 1 -1

1 Hemodialysis with ultrafiltration (may be T 1

ume Chronic renal failure

+ Dialysis procedures

Isolated ultrafiltration *

affected by dialysate buffer) T = Increase; 1 = decrease; - = No change; V = variable. - Depending on rate of volume removal, osmolality, changes, presence

of myocardial dysfunction.

244 Travis and Henrich

milieu or the imposed interplay of factors common to dialysis patients remains to be determined.

Coronary Artery Disease. As noted at the outset of this discussion, the prevalence of coronary artery disease is high in patients with chronic renal failure. However, Rostand et al. (27) have noted that the development of ischemic heart disease in dialysis patients without evidence of ischemia prior to di- alysis initiation did not affect long-term outcome. Myocardial oxygen consumption is increased in di- alysis patients because of an increased heart rate, increased ventricular wall tension (afterload), an in- creased ventricular muscle mass (hypertrophy), and anemia.

Several hemodynamic patterns of ischemia have emerged in ESRD patients (28, 29). Small ischemic areas do not appear to change ventricular filling pressures, mean arterial pressure, and cardiac output whereas larger areas of ischemia cause increases in LVEDP, mean arterial pressure (MAP) and cardiac output. Still larger areas of ischemia create an in- crease in LVEDP but a decrease in MAP and cardiac output. Of interest are the recent data of Opsahl et al. (30)

who have noted an acceptable risk of bypass grafting (operative mortality of 2.6%) with improved long- term survival in ESRD patients with ischemic heart disease (30). A recent study suggested a greater in- hospital morbidity in dialysis patients undergoing coronary bypass surgery when compared to age and disease-matched nonuremic controls (3 1).

Uremic Cardiomyopathy. Despite the sugges- tion of a uremic toxin causing myocardial dysfunc- tion¶ conclusive clinical or experimental evidence is still lacking. A carefully studied animal model of ESRD did not provide evidence for a direct effect of uremia on myocardial hnction (32). It has been difficult in humans to separate any individual effects of a putative uremic toxin on myocardial function from the premorbid conditions known to affect per- formance (hypertension, ischemic disease, etc.).

Pericardial Disease. Pericardial effusions occur in approximately 10 to 20% of asymptomatic ESRD patients; these become hemodynamically significant in 4%. When tamponade occurs, a rising intraper- icardial pressure equilibrates with LVEDP and limits LVEDV and stroke volume; cardiac output can then be maintained only by an increase in heart rate. Blood pressure falls once cardiac output and vaso- regulatory mechanisms are incapable of augmenting perfusion. Hemodialysis in t h i s situation can cause a sharp collapse in blood pressure by diminishing central blood volume, LVEDV, stroke volume, and by decreasing peripheral vascular resistance.

Miscellaneous. Aortic stenosis from valvular calcification has been associated with mitral annular calcification and is more common in dialysis pa- tients. Calcification of the conduction system may provoke rhythm disturbances and loss of atrial and ventricular synchronization, reducing stroke volume and cardiac output.

Patients with ESRD also have important defects within the autonomic reflex arc (33-36). Inadequate

compensatory tachycardia and inadequate incre- ments in peripheral vascular resistance during di- alysis make these patients prone to frequent episodes of hypotension.

In some studies, serum parathyroid hormone has been shown to have a cardiodepressant action. U1- mann et al. (37) noted diminished cardiac resmn- siveness to adrenergic stimulation in a patient which improved with removal of a parathyroid adenoma. This observation was corroborated by Drueke et al. (38) who noted improved cardiac performance after parathyroidectomy in hemodialysis patients. How- ever, a recent study which compared myocardial contractility before and after parathyroidectomy failed to show a significant improvement (39).

Summary Cardiac performance during hemodialysis is de-

pendent on preexisting conditions (i.e., coronary artery disease, myocardial hypertrophy, LV compli- ance, anemia, hypertension, etc.) and the hemody- namic alterations caused by the dialysis procedure itself (osmotic shifts, ionized calcium changes, etc.). Clinical hemodynamic investigations of cardiac per- formance during uremia have been hampered by the difficulty in isolating individual parameters of ven- tricular function. Myocardial reserve in dialysis pa- tients is often reduced because of antecedent is- chemic disease, hypertension, and the presence of autonomic dysfunction in many patients. Rapid vol- ume losses or gains are likely to be less well tolerated with resultant hypotensive syndromes or pulmonary edema as the result. The controlled volume loss achievable with newer dialysis machines, the use of higher dialysate sodium concentrations, and the wider availability of erythropoietin may improve the tolerance to the procedure for many patients.

References I. Gurland HJ, Brunner FF', V Kehn H, et al: Combined report on regular

dialysis and transplantation in Europe. Proc Eur Dial Transplant Assoc 10:17, 1973

2. Linder AL, Charm B, Herrard DJ, Scribner BH: Accelerated athero- sclerosis in prolonged maintenance hemdialysis N Engl J Med

3. Burke JF, Francos GC, Moore LL, et al: Accelerated atherosclerosis in chronic dialysis patients-another look. Nephron 21:181-185, 1978

4. Nicholls AJ, Edward N, Catto GRD, Engeset J: Accelerated atherosdc- rosis in long-tenn dialysis and renal transplant patients: Fact or fiction? Lancer 1:276-279, 1980

5. Rostand SG, Kirk KA, Rutsky EA: Relationship of coronary risk factors to hemodialysis-associated ischemic heart disease: Kidney Inl 22304-308, 1982

6. DefaZio V, Christenen RC, Regan TJ, et al: Circulatory changs in acute glomerulonephritis. Circulation 2 0 190, 1959

7. Agrest A, Fmkielman S: Hemdynamics in acute renal failure. F'atho- genesis of hyperkinetic circulation. Am J Cardiol19213-2 19, 1967

8. Anthonisen P, Holst E Determination of cardiac output and other hemodynamic data in uremic patients using dye-dilution technique. &and J Clin Lab Invest 12:481, 1960

9. Mosten JW. Even JL, Hobika GH, et al: The haemodynamic response to chronic renal failure as studied in the azotaemic state: Er J Arms- rhesiol42397-41 I , 1970

10. Neff MS, Kim KE, Persoff M, Onesti G Hemdynamics of uremic anemia. Circulation 43:876-882, 197 I

1 1. Kim KE, Onesti G, Schwartz AB, el al: Hemdynamics of hypertension in chronic end-stage renal disease. Circulation 46:456-465, 1972.

12. Gibson DG: Hemdynamic factors in the development of acute pul-

290697-701, I974

HD-WHAT AFFECTS CARDIAC PERFORMANCE? 245

monaryedema in renal failure: h n c e t 21217-1223. 1966 13. Kramer W. Wizemann V. Lammlein G, et al: Cardiac dysfunction in

patients on maintenance hemodialysis. Contrib Nephrol 52: 1 10-1 24, I986

14. Del Greco F, Simon NM, Roguska J, et al: Hemodynamic studies in chronic uremia. Circulation 40:87-96, 1969

IS. Goss JE, Alfkey AC, Vogel HK. et al: Hemodynamic changes during hemodialysis. Trans Am Soc Arti/lntem Organs I3:68-74, 1967

16. Rutsky EA, Rostand SG. Cardiac performance and coronary risk in chronic hemodialysis patients. Kidney 1 6 1-6, 1983

17. Fernando HA, Friedman HS, Zaman Q, et ak Echocardiographic assessment of cardiac performance in patients on maintenance hemo- dialysis. Cardiovasc Med 4459, 1979

18. Chen TS, Friedman HS, DeI Monte M, and Smith Al: Hemodynamic changes during dialysis. Prtx Dial Transplant Fonun 9:66-71,1979

19. Rouby JJ, Rottenbourg J, Durande JF', et al: Hernodynamic change induced by regular hernodialysis and sequential ultrafiltration heme dialysis A comparative study. Kidney Int 17:801-8 10, 1980

20. Bergstrom J. WehIe B, Asaba H, et al: Effect of ultrafiltration and dialysis on blood pressure and cardiic output. Kidney Inr 12477,1977

2 1. Wehle B, Asaba H. Casterfon J, et al: The influence of dialysis fluid composition on the blood pressure response during dialysis. Clin Ne- phrol1062-66, 1978

22. Nixon JV, McPhaul JJ, Mitchell HC, Henrich WL: Effects of hemo- dialysis on left ventricular function. J Clin Invest 71:377-384, 1983

23. Henrich W L Hunt JM, Nixon J V An increase in ionized calcium improws left ventricular contractility during hemodialysis. N €ngl J Med 310:19-23, 1984

24. Lang RM, Fellner SK, Neumann A: Left ventricularcontractility varies directly with blood ionized calcium. Ann Intern Med 108524-529, 1988

25. Bristow MR, Schwartz HD, Biretti G. et al: Ionized calcium and the heart Elucidation of in vivo concentration-response relationships in the open-chest dog. Circu Res 41565, 1977

26. Rambausek M, Mann JFE, Mall G, et al: Cardiic findings in experi- mental uremia. Contrib Nephrol52:125-133, 1986

27. Rostand SG. Gretes JC, Kirk KA, et al: Ischemic heart disease in patients with uremia undergoing maintenance hemodialysis. Kidney Int I6:600-6 I I , 1979

28. Johnson RA. Pohost GM, Strauss HW. et al: Cardiac 20'TI rediibu- tion aRa exercise. Relationship to ischemia-induced changes in left ventricular filling pressure and to angiographicextent of coronary artery disease (Abstract). Clin Res 26241A, 1978

29. Sharma B. Goodwin JF, Raphael MS, et ak Lefi ventricular angiogra- phy on exercise. A new method of assessing left ventricular function in ischemic heart disease. Br Heart J 385963,1976

30. Opsahl JA, Huseby DG, Helseth HK, et al: Coronary army bypas surgery in patients on maintenance dialysis Long-term survival. Am J Kidney Dis 12271-274, 1988

31. Deutsh E, Bemstein RC, Addonido VP, Kussrnaul WG. Coronary artery by-pass surgery in patients on chronic hernodialysis Ann Intern Med 110369-372, 1989

32. Lubbecke F, Steudle V, Schaper J, Wizemann V Experimental uremic cardiornyopathy-fact or fiction? Contrib Nephrol52134-145, 1986

33. Ewing DJ, Winney R: Autonomic function in patients with chronic renal failure on intermittent haemcdialysis. Nephron 15424429.1975

34. Lilley IS, Golden J, Stone RA. Adrenergic regulation of blood pressure in chronic renal failure. J Clin Invest 57:1190-1200, 1976

35. C a m p VM, Romoff MS, Levitan D, et al: Mechanisms ofautonomic nervous system dysfunction in uremia. Kidney Int 20246-253, 1981

36. Mallamaci F, Zoccoli C, Cicamlli M, Briggs J: Autonomic function in uremic patients trtated by hernodialysis or CAPD, and in transplant patients. Clin Nephrol25: 175-180, 1986

37. Ulmann A, huekc T, Zing& J, Crosnia J: The response of heart rate to isoproterenol in hernodialyzed patients before and after para- thyroidectomy. Clin Nephrol7:58-60, 1977

38. Drueke T , Fleury J, Toure Y, et al: Effect of parathyroidectomy on left ventricular function in hemodialysis patients. Lancet: 1: I 12-1 14, 1980

39. Zucchelli P, Santoro A, Zucchelli A, Spongano M, F m G. Long- term effects of parathyroidectomy on cardiac and autonomic nervous system functions in haemodialysis patients. Nephrol Dial Transplanr 3:45-50. 1988

Acute Peritoneal Dialysis: 1938

In 1938, Jonathan Rhoads of the University of Pennsylvania performed acute peritoneal dialysis in two patients. Six exchanges of 1.5 liter took 2% hours; blood urea nitrogen dropped about 30 mg% with each dialysis. One patient was dialyzed three times, the other patient only once before expiring; transient improvement in mental status was seen in both. Rhoads was unable to remove excess fluid, despite the addition of hypertonic glucose to the dialysis fluid; he proposed the addition of "a nondiffusible solute such as acacia in sufficient amounts to counteract the oncotic pressure of the serum proteins." The safety of peritoneal puncture and introduction of a cannula was a matter of some concern at the time:

"There is some justifiable hesitance in performing abdominal punctures, as fatalities have been reported. . . . In both of the patients reported here, the visceral peritoneal surfaces were carefully examined at autopsy for evidence of injury but none was found. In both cases the peritoneal surfaces were clean and glistening."

In commenting on his trial of peritoneal dialysis, Rhoads concluded: "Both of these patients were shown at autopsy to have chronic glomerulonephritis and accord- ingly were unsuitable for treatment by peritoneal lavage. They, therefore, cannot properly be used for evaluation of the clinical results of this method. They do demonstrate, however, that the peritoneal cavity can be used in patients as a dialyzing membrane and that in the presence of high blood urea nitrogen concentrations substantial quantities of urea can be removed. . . . The method is recommended for further trial in cases of acute renal failure in which the prognosis for the recovery of the kidneys is fair, provided the patient survives a limited period of renal insufficiency."

Rhoads JE: Peritoneal lavage in t h e treatment of renal insuffiency. Am J MedSci 196:642-647, 1938 (used with permission)