Hepatorenal Syndrome. Studies of the Effect of Vascular Volume and Intraperitoneal Pressure on Renal and Hepatic Function

Cade, Robert; Wagemaker, Herbert; Vogel, Stephen B.; Mars, Donald R.; Hood-Lewis, Dennis; Privette, Malcolm; Peterson, John C.; Schlein, Edward; Hawkins, Richard A.; Raulerson, Daniel; Campbell, Kelly

doi:10.1016/s0022-5347(17)43323-4

Cited by 10 publications

(19 citation statements)

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“…Vasodilatation associated with general anaesthesia may result in renal hypoperfusion and the development of pre-renal renal failure. Any acute deterioration in liver function can lead to the hepatorenal syndrome, 6 caused by renal hypoperfusion, portal hypertension, intra-abdominal hypertension, and nephrotoxins alone or in combination. The development of hepatorenal failure will necessitate postoperative haemodialysis and carries a poor prognosis.…”

Section: Renal and Metabolicmentioning

confidence: 99%

Anaesthesia for patients with liver disease

Vaja

McNicol

Sisley

2010

Continuing Education in Anaesthesia Critical Care & Pain

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Section: Renal and Metabolicmentioning

confidence: 99%

Anaesthesia for patients with liver disease

Vaja

McNicol

Sisley

2010

Continuing Education in Anaesthesia Critical Care & Pain

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“…Physiology DECREASED VENOUS RETURN (PRELOAD). Venous return (preload) is decreased through several mecha-The main physiologic consequences of increased nisms [13,16,17,[21][22][23]49,56,59,61,[86][87][88][89]. Elevated IAP are summarized in Table 1.…”

Section: The Peritoneum Itself May Absorb Huge Amountsmentioning

confidence: 99%

“…Removal of ascites in Fluid overload, on the other hand, contributes to intra-abdominal volume and pressure augmen-cirrhotic patients to decrease IAP has been associated with a dramatic improvement in renal function tations. In an individual patient, the effects of increased IAP are not isolated but may be [28, 85,89], cardiac performance, and hepatic perfusion [14,56,88]. Sudden removal of a large volume of superimposed on multiple coexistent factors.…”

Section: (B)mentioning

confidence: 99%

The Compartment Syndrome of the Abdominal Cavity: A State of the Art Review

Wittmann

Iskander

2000

J Intensive Care Med

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Abdominal compartment syndrome gains increasing recognition. It impairs physiology and requires treatment. It occurs more commonly with acute rather than chronic abdominal hypertension. Functional impairments involve the cardiovascular system, respiratory system, hepatic, renal, and gastrointestinal function, and intracranial pressure. Abdominal hypertension decreases venous return, increases systemic vascular resistance and intrathoracic pressure, and therefore reduces cardiac output. It also adversely affects cardiovascular monitoring. In the presence of increased abdominal pressure, atelectasis and pneumonia are likely to develop and impaired ventilation may lead to respiratory failure. Also, blood flow to the liver and kidney may be reduced, resulting in functional impairment of both organs. The adverse effects on gastrointestinal function result from impairing lymphatic, venous, and arterial flow. Anastomotic healing may become a problem under these circumstances. Decreased venous return through the inferior vena cava in obese patients may lead to venous stasis ulcers and hemorrhage. The correlation of increased intracranial pressure and intra-abdominal pressure may be a problem for trauma patients with simultaneous injuries to the head and the abdomen. There are three severity grades of increased intra-abdominal pressure: Acute sustained elevation of intra-abdominal pressure above 10–20 mmHg is called mild abdominal hypertension. Physiologic effects are generally well compensated and usually clinically nonsignificant. Nonoperative therapy may be required. Moderate hypertension is defined as sustained elevation of 21–35 mmHg. Therapy is generally necessary. Surgical abdominal-decompression may be critical. Severe hypertension or abdominal compartment syndrome is defined as sustained elevation above 35 mmHg. Operative decompression is always indicated. The gap between the abdominal wound edges must be temporarily covered to prevent fascia retraction and formation of a huge hernia. All detrimental effects of elevated intra-abdominal pressure and the methods and benefits of its decompression have been well studied, both in the laboratory and in clinical practice. Diagnostic suspicion may be confirmed with objective measurements of intra-abdominal pressure to select patients who may benefit from decompression. Operative decompression is achieved by abdominal fasciotomy and covering the fascial gap with mesh made of Marlex®, Gore-Tex®, silastic, or by a Velcro-like closure mesh (artificial bur). All meshes help to effectively decompress the abdomen. The artificial bur offers further advantages by permitting successive reapproximation of the fascia until final fascial closure, and avoiding the fistula and hernia formation seen with the other meshes.

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“…Venous return (preload) is decreased through several mechanisms [13,16,17,21–23,49,56,59,61,86–89]. Elevated IAP is directly transmitted to large retroperitoneal veins, resulting in the caudal pooling of blood and decreased inferior vena cava flow [59] ( Fig 6).…”

Section: Physiologymentioning

confidence: 99%

“…Nonoperative decompression has been reported mainly for cirrhotic patients with ascites. Removal of ascites in cirrhotic patients to decrease IAP has been associated with a dramatic improvement in renal function [28,85,89], cardiac performance, and hepatic perfusion [14,56,88]. Sudden removal of a large volume of peritoneal fluid is hemodynamically safe in patients who are not volume depleted [111].…”

Section: Therapeutic Decompressionmentioning

confidence: 99%

The Compartment Syndrome of the Abdominal Cavity: A State of the Art Review

Wittmann¹,

Iskander²

2000

J Intensive Care Med

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Abdominal compartment syndrome gains increasing recognition. It impairs physiology and requires treatment. It occurs more commonly with acute rather than chronic abdominal hypertension. Functional impairments involve the cardiovascular system, respiratory system, hepatic, renal, and gastrointestinal function, and intracranial pressure. Abdominal hypertension decreases venous return, increases systemic vascular resistance and intrathoracic pressure, and therefore reduces cardiac output. It also adversely affects cardiovascular monitoring. In the presence of increased abdominal pressure, atelectasis and pneumonia are likely to develop and impaired ventilation may lead to respiratory failure. Also, blood flow to the liver and kidney may be reduced, resulting in functional impairment of both organs. The adverse effects on gastrointestinal function result from impairing lymphatic, venous, and arterial flow. Anastomotic healing may become a problem under these circumstances. Decreased venous return through the inferior vena cava in obese patients may lead to venous stasis ulcers and hemorrhage. The correlation of increased intracranial pressure and intra‐abdominal pressure may be a problem for trauma patients with simultaneous injuries to the head and the abdomen. There are three severity grades of increased intra‐abdominal pressure: Acute sustained elevation of intra‐abdominal pressure above 10–20 mmHg is called mild abdominal hypertension. Physiologic effects are generally well compensated and usually clinically nonsignificant. Nonoperative therapy may be required. Moderate hypertension is defined as sustained elevation of 21–35 mmHg. Therapy is generally necessary. Surgical abdominal decompression may be critical. Severe hypertension or abdominal compartment syndrome is defined as sustained elevation above 35 mmHg. Operative decompression is always indicated. The gap between the abdominal wound edges must be temporarily covered to prevent fascia retraction and formation of a huge hernia. All detrimental effects of elevated intra‐abdominal pressure and the methods and benefits of its decompression have been well studied, both in the laboratory and in clinical practice. Diagnostic suspicion may be confirmed with objective measurements of intra‐abdominal pressure to select patients who may benefit from decompression. Operative decompression is achieved by abdominal fasciotomy and covering the fascial gap with mesh made of Marlex®, Gore‐Tex®, silastic, or by a Velcro‐like closure mesh (artificial bur). All meshes help to effectively decompress the abdomen. The artificial bur offers further advantages by permitting successive reapproximation of the fascia until final fascial closure, and avoiding the fistula and hernia formation seen with the other meshes.

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Hepatorenal Syndrome. Studies of the Effect of Vascular Volume and Intraperitoneal Pressure on Renal and Hepatic Function

Cited by 10 publications

References 0 publications

Anaesthesia for patients with liver disease

Anaesthesia for patients with liver disease

The Compartment Syndrome of the Abdominal Cavity: A State of the Art Review

The Compartment Syndrome of the Abdominal Cavity: A State of the Art Review

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