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One hundred thirty-nine patients with disordered nitrogen metabolism received an intravenous solution of essential L-amino acids and hypertonic dextrose to provide parenteral nutrition in the presence of either acute renal failure, “hepatorenal syndrome,” chronic hepatic insufficiency without renal failure, or azotemia resulting from a variety of other causes. Infusions were managed by routine hyperalimentation technics, modified somewhat to avert potential metabolic side effects. Clinical and metabolic results attributable to the therapy included improved nutritional status and salutary serum electrolyte changes. Complications of therapy were few in number; notable was hyperglycemia which was easily managed in most instances. The capacity to safely deliver intravenous nutrients to patients even with marked disturbances in hepatic or renal function is clearly established.

A case of juvenile angiofibroma occurring in a male patient of 49 years is described. Histopathology and oncogenesis are discussed.

Convulsions during anesthesia are rather uncommon but it is important for physicians to be on the alert to treat these unfortunate occurrences and prevent them if possible. Six convulsions during anesthesia were encountered in one year. The etiology of these convulsions is extremely vague. The literature is replete with possible causes, many of which contradict each other, thereby making the situation more confusing. Despite lack of knowledge concerning the causative factors, we should give strict attention to the preoperative care of our patients, particularly those who are acutely ill and toxic, thereby very likely lessening the number of convulsions during anesthesia. The authors recommend the prompt administration of sodium pentothal as advocated by Lundy. Heretofore the mortality in patients having convulsions during anesthesia was extremely high. With sodium pentothal at hand, this figure should be lower. There was only one death among the six patients herein presented and this was attributable, not to the convulsion but to hepatorenal failure on the fifth postoperative day.

SummaryThe effects of 24 hr intravenous infusion of dopamine in 9 cirrhotic patients without azotemia and one patient with mildly elevated BUN were studied. Dopamine (3, 4-dihydroxyphenylethylamine) 2 μg/kg/min produced statistically significant decrease in creatinine clearance and urine osmolarity, and an increase in urinary sodium excretion of borderline significance. These could be attributed to “shunting” of blood from the renal cortex to the medulla brought about by dopamine. This effect was reversible when the drug infusion was discontinued. The therapeutic value of dopamine in hepatorenal syndrome is therefore being questioned.

The role of the kidney in hepatic disease and in gout has been surveyed. Kidney involvement is more common but less severe in hepatic disease, whereas it is less common but more severe in gout. The underlying pathology of the kidney lesions in both diseases (including studies by electron microscopy and immunofluorescence) is presented, with emphasis on the role this pathologic substratum plays in the renal insufficiency. The clinical aspects, including the diagnostic approach and therapeutic management of the "hepatorenal syndrome" and "gouty kidney" are discussed, as are the prognostic implications of the natural history of these "complications" and measures aimed at their prevention.

An attempt is made to unify the pathophysiology of the cerebral, cardiovascular, and renal complications of hepatic failure by postulating the accumulation of false neurochemical transmitters in the presynaptic storage sites of the peripheral and central adrenergic nervous system. Such an hypothesis is consistent with many widely accepted clinical and biochemical observations previously made about hepatic failure, hepatic coma, and the hepatorenal syndrome. It may explain the recently described beneficial effects of L-dopa on the mental and circulatory status of patients in hepatic failure and the occasionally successful treatment of the hepatorenal syndrome with large doses of metaraminol or other alpha-adrenergic amines. Experimental findings obtained in both laboratory animals and patients are presented.

1. 1. Seventy-five cases of postabortal infection with Clostridium welchii are presented. These occurred from 1948 to 1952 at the Maternity Hospital in Santiago, Chile. 2. 2. The incidence of this infection at this hospital among all patients with abortion was 1 in 307. 3. 3. The symptoms and clinical course of these cases are described. The diagnostic triad of hemoglobinuria, hemoglobinemia, and a deep bronze icterus leaves no difficulty in the diagnosis of this disease. 4. 4. The course of the disease is described as occurring in two phases, the icterohemolytic syndrome and the hepatorenal syndrome. 5. 5. The mortality rate was 73.3 per cent, with a decrease in mortality rate from 87.5 per cent early in the series to 68.7 per cent in the last year. 6. 6. Twenty-three (30 per cent) of these patients developed anuria; 94.6 per cent had oliguria some time during the course of their illnesses. 7. 7. Laboratory and pathological findings are described. 8. 8. Treatment was directed along three basic lines, removing the focus of infection in the uterus, specific treatment with Perfringens antitoxin and antibiotics, and supportive treatment. 9. 9. Although the outcome of any given case depended primarily on the virulence and toxicity of the organism, treatment as outlined appeared to offer a better chance of survival. 10. 10. The serious abortion problem in Chile is decried and a plea for preventive measures to curtail it made.

1. Experimental acute intestinal distention in nembutalized dogs caused a reflex inhibition of the bile flow. Intraenteric pressures of 20 and 40 mm. of mercury resulted in a decrease in the bile flow of 7 to 42 per cent below the control level. 2. A decrease in the portal blood flow and oxygen supply to the liver produced by distention of the entire intestine to pressures of 70 mm. of mercury caused a further decrease in bile flow in 4 of our dogs. Oxygen therapy lessened this inhibition in all of the dogs treated. 3. Nervous reflex inhibition of the flow of urine did not occur upon distention of the small intestine to pressures of 20, 40, 60 and 90 mm. of mercury. An increase in urine flow from 11 to 81 per cent occurred. This was attributed to an increased blood flow through the kidneys. 4. The blood pressure was not significantly altered by distention of the small intestine. 5. The depth of respiration was decreased and the rate was increased by distention. Oxygen therapy decreased the respiratory rate and lessened the depression of bile flow produced by distention of the small intestine. 6. Inhibitory nervous reflexes, decreased blood flow and anoxemia probably are factors involved in decreasing liver function and thereby make the liver more susceptible to damage in cases of intestinal distention. 7. Inhibition of liver function probably precedes inhibition of kidney function in the hepatorenal syndrome of intestinal obstruction.

Historical data about the hepatorenal syndrome is discussed. Clinical and experimental studies are reported. Some mechanisms of acute functional renal failure are discussed. The hepatorenal syndrome as an answer to shock and stress is pointed out.

1. Inhalation of 15 per cent oxygen in nitrogen for 30 to 45 minutes resulted in a 16 to 50 per cent decrease in the flow of bile below normal and a 13 to 69 per cent decrease in the flow of urine below normal in 10 nembutalized dogs. 2. Inhalation of mixtures of 10 and 5 per cent oxygen with nitrogen caused a further decrease in the flow of bile and urine. Acholia developed in 2 dogs and anuria in 5 dogs. 3. The inhalation of 100 per cent oxygen for 30 to 45 minutes after the anoxemia resulted in an increase in the flow of bile and urine above that observed during the anoxemia. In 3 dogs the flow was increased above the normal control level. 4. Mild anoxemia may be a predisposing factor in the hepatorenal syndrome of intestinal obstruction, hyperthyroidism and burns. The moderate inhibition of liver and kidney function may make these organs more susceptible to other injurious agents. 5. Severe anoxemia may be a direct causative factor because it produces a severe impairment of liver and kidney function and in some instances it may produce an acholia and anuria.

We have utilized new methods of dialyzer-augmented whole blood and plasma exchange tranfusion in the treatment of hepatic coma. The method employs the new fast flow Buselmeier shunt so that the exchange can be done from a peripheral radial artery shunt site rather than a shunt site in a more major vessel, such as the brachial artery. The method employs in-line dialysis of citrated (CPD) blood or plasma to normalize pH, electrolytes, and blood sugar while infusion heparinization decreases heparin requirements. The application of a single roller pump to the administration and withdrawal lines (placed in opposite directions) helps equalize inflow and outflow where whole blood exchange is done while identical opposing pumps accomplish the same with plasma exchange. The administration of albumin and metaraminol bitartate prevents hypotension due to fluid shifts or compartmental venous dilatation. A closed circuit which does not require disconnection throughout the 30- 60-minute whole blood exchange or the 2 1/2-hour plasma exchange decreases the risk of septic contamination to both medical staff and patients.

In a ten-year retrospective study 15 cases of spontaneous bacterial peritonitis were identified. All patients had cirrhosis and ascites. Abdominal pain was present in all and abdominal tenderness in 11. Diagnosis was established by paracentesis with the finding of either an elevated ascitic fluid cell count (>300 WBC/mm3) in 13 cases or organisms and numerous neutrophiles on gram stain in 6 cases. On ascitic fluid cultureE coli was the most common organism isolated in 6 cases, klebsiella was isolated in 3 cases, andDiplococcus pneumoniae (D. pneumoniae) in 2 cases. Positive blood cultures were obtained in 60% of the cases. Three patients responded to therapy, including antibiotics, and survived to leave the hospital. No features unequivocally differentiated the survivors. The nonsurvivors died from complications of advanced liver disease including hepatic coma, hepatorenal syndrome, and esophageal variceal hemorrhage. Spontaneous bacterial peritonitis is a potentially treatable cause of deterioration in the patient with cirrhotic ascites. Because of its varied presentation it may escape recognition despite ease of diagnosis. Prompt recognition requires awareness of this entity.

A single dose of endotoxin given to rats with obstructive jaundice produced death with intravascular coagulation. This action was apparently due to delayed clearance of endotoxin from the circulation. The finding is relevant to “hepatorenal failure,” which can be caused by bacteraemia after biliary tract operations.

During the last year, seven men bleeding from varices and one with intractable ascites underwent, either electively or as an emergency (three), mesocaval shunting with the use of homologous vena cava (H graft). Autopsy in two patients, who died a few weeks postoperatively from hepatorenal failure, showed that the grafts were open. Splenoportography some months later demonstrated "balanced" shunts in five of the six survivors. The exception underwent a repeat procedure and now has a functioning homograft. A death from hematemesis 11 months after surgery was associated with obliteration of the shunt, possibly from compression between the pancreas and duodenum. Since one of the operative fatalities sustained pancreatic injury, the graft is now brought below the duodenum. H-grafting enhances the many technical advantages of mesocaval shunting by eliminating the need to uproot the inferior vena cava. The question whether venous homografts stay open in man remains.

A kidney from each of five patients and both kidneys from a sixth patient dying with the hepatorenal syndrome (severe hepatic failure, oliguria, azotemia, hyponatremia and a urinary sodium of less than 5 mEq per day) were transplanted into seven patients with end-stage kidney disease whose liver function was normal. Diuresis and improvement of renal function occurred in all but one recipient. Because of postoperative complications, two kidneys were removed after diuresis had occurred. Four transplanted kidneys achieved stable function for six months or longer, with creatinine clearances of 25, 42, 50 and 52 ml per minute. The hepatorenal syndrome is functional and potentially reversible.

Excerpt After exsanguinotransfusion had been tried and abandoned during the 17th century it was not used again until recently, when total replacement of blood was reintroduced by American clinician...

A relationship between liver disease or damage and kidney function has been observed and was termed the hepatorenal syndrome. 1-3 The exact nature of this relationship has never been delineated and theoretically could involve insufficient liver function; circulatory insufficiency, such as dehydration and hypovolemia; massive outpouring of protoplasmic catabolites from disintegrating liver; or bacterial infection. Shock, alone or combined with any of the above, may be the precipitating factor. 4,5 It is the purpose of the present study to examine whether severe hepatic damage, in the form of massive liver necrosis, is capable of suppressing renal performance completely or partially, in the absence of dehydration or shock. In another publication 6 it was demonstrated that, in the same experimental model 7 used for the present work, infection of the devitalized liver and hepatic insufficiency 8 play no significant role. Materials and Methods Twelve apparently healthy mongrel dogs of either sex

Three patients with progressive renal failure and advanced hepatic insufficiency due to cirrhosis of the liver underwent orthotopic liver transplantation. All three patients had immediate improvement in hepatic function and within two weeks after liver replacement regained nearly normal kidney function. However, the renal recovery was delayed in each case, and its course was not uniform. Plasma renin activity was high, and renin substrate was low before transplantation in one case in which these measurements were obtained; both returned to normal soon after liver replacement. (N Engl J Med 289:1155–1159, 1973)