The Child-Pugh score considers the patients bilirubin, albumin, INR, presence or absence of encephalopathy, and presence or absence of ascites. In this patient prior to surgery his breakdown was as follows:
Bilirubin: 4.2 mg/dl (greater than 3 mg/dl = 3 pts)
Albumin: 2.4 g/dl (<2 .8="" dl="3" g="" p="" pts="">INR: 1.4 (<1 .7="1" p="" pt="">No ascites = 1 pt
encephalopathy (medically controlled) = 2 pts
His total score is 10 pts which makes him a grade C. Life expectancy is 1 to 3 years and mortality with major abdominal surgery is 82%. Obviously, preoperative mortality in these patients is extreme, making elective surgery an unlikely choice. However, this was essentially urgent life potentially life saving surgery, and furthermore, was not major abdominal, but an IM nail.
Child-Pugh Calculations
| Points* | |||
|---|---|---|---|
| 1 | 2 | 3 | |
*CTP score is obtained by adding the score for each parameter.
CTP class: A = 5-6 points (predicted mortality major abdominal surgery ~10%) <5 p="">B = 7-9 points (predicted mortality major abdominal surgery- ~25%) C = 10-15 points (predicted mortality major abdominal surgery greater than 50%)
Making a determination of the severity of a patient's liver disease is a challenging problem. It is important to quickly classify a patient presenting for surgery as compensated liver cirrhosis or decompensated cirrhosis.
Compensated cirrhosis is a patient that does not have ascites, jaundice, encephalopathy, or variceal bleeding. If any of these are present, it is considered decompensated cirrhosis. In patients with compensated cirrhosis, the Child-Pugh classification can be a good guide to the severity of their disease. A Recent systemic review found the Child-Pugh score was still significant among the predictors of death despite the absence of ascites, encephalopathy and jaundice in the patients with compensated cirrhosis, because its laboratory components, bilirubin, albumin and prothrombin time continued to be among the most frequent predictors, indicating that even subtle abnormalities in these laboratory parameters are predictive of death [1]. The Child-Pugh score was originally designed about 30 years ago to predict mortality with surgery for portal hypertension. Since this time, the MELD score was created to predict the mortality following a transjugular intrahepatic shunt procedure (TIPS). Later it was adapted to risk stratify patients on the waiting list for liver transplantation. The MELD score, in addition to considering the INR, bilirubin, and albumin, considers the patients creatinine which is highly correlated with morbidity. Another smaller study in hip arthroplasty patients stated the following, " Of the twelve variables evaluated in our series, a high level of creatinine was found to be the only risk factor associated with perioperative mortality. However, combining all of the categories included in the Child-Pugh scoring system, a higher Child-Pugh score was another important risk factor of perioperative morbidity. " [2] Therefore, when using the child-Pugh score to evaluated potential risk in a patient, looking for creatinine greater than 1.5 mg/dL is advisable as it likely contributes significantly to overall mortality.
Even better, however, may be using an online calculator to determine the MELD score. The MELD score has the advantages of objectivity, weighing of the variables, and does not rely on arbitrary cutoff values as in the case of the Child-Pugh score. Each one-point increase in the MELD score makes an incremental contribution to risk, thereby suggesting that the MELD score increases precision in predicting postoperative mortality. Here is a link to a web based calculator (save it as an icon on your phone for ease of use).
More recently, studies have tried to determine how the MELD score can predict risk associated with other types of surgery. In 2005, a retrospective review of 140 patients undergoing surgery found that with a MELD score of 5 to 20, there was a 1% increase in mortality per MELD point increase. After 20, the risk of mortality increased 2% for each point increase in the MELD score. [4] In this study, they looked at 30 day mortality after surgery, with a 5% mortality rate with a MELD of 5 pts. A larger study, also retrospective, found that with a MELD less than 7, the mortality rate was 5.7%. A MELD score of 8 to 11 increased the mortality rate to 10.3% and with a MELD of 12 to 15 had a mortality rate of 25%. [5] This was a review with open abdominal, orthopedic and cardiovascular surgery.
A significant issue related to anesthesia is increased intrapulmonary shunting that can occur resulting in low oxygen saturation. If significant, this can lead to hepatopulmonary syndrome (HPS). This diagnosis typically requires a saline bubble test using echocardiography where agitated saline is injected IV. These patients will have dyspnea and hypoxemia when sitting upright, which is relieved by lying flat (orthodeoxia). [3] While this may seem to be of benefit to us since we require the patient be in the supine position these patients tend to be very sick and thus any elective case should be postponed for further evaluation. The key to an anesthetic in a patient with significant cirrhosis who is compensated, is to avoid moving to a decompensated state. Since these patients often have portal hypertension (portal vein pressure greater than 10 mmHg), blood flow is often very dependent on the hepatic artery and thus MAP. Since all anesthetics (general or spinal) can reduce MAP, hepatic artery blood flow is reduced, and the liver is at risk. This risk is increased dramatically in abdominal surgery, particularly with laparoscopy where pressure is increased intraperitoneally while MAP is decreased. In advanced cirrhotic liver disease this vulnerability to anesthetics is greatly enhanced due to pathophysiological changes that accompany worsening liver disease. This can include a decrease in the effective circulating plasma volume due to several factors: 1) increase in splanchnic blood pooling as a result of increased resistance of blood flow through the cirrhotic liver and 2) vasodilation of the systemic and splanchnic circulation from increased production of vasodilators. The baroreceptors sense a decrease "load" and thus the SNS, the renin-angiotensin-aldosterone system (RAAS), are activated resulting in significant vasoconstriction in other parts of the body. Furthermore, a non osmotic release of vasopressin occurs, further enhancing water retention and vasoconstriction. The end result of all of the forces of hepatic cirrhosis with significant liver congestion, is a state of increased cardiac output, decreased SVR, hypotension, but potentially intense vasoconstriction of renal arteries. It has been demonstrated that as the liver disease progresses, splanchnic vessel vasocodilation increases, and this correlates directly with the low SVR, hyperdynamic state of liver failure with cirrhosis. It can also be demonstrated that femoral artery and upper extremity arterial flow decreases in sync with increased renal artery vasoconstriction and flow. The primary cause of this is unclear, but studies suggest that the renal sympathetic system plays a contributory role in renal vasoconstriction in the face of mesenteric vasodilation. What is clear from the work done in animal and human models, is that as the cirrhotic liver worsens, there is a larger impact on blood pooling and vasodilation of the mesenteric vasculature which is the primary culprit in the worsening low SVR hyperdynamic state known to accompany advanced liver cirrhosis. As this progresses, renal sympathetic tone increases, leading to greater and greater renal artery vasoconstriction until it manifests itself clinically as hepatorenal syndrome, a harbinger of death for most liver patients.
Therefore, renal function is very important to evaluate prior to anesthesia in patients with advanced liver disease (i.e Child-pugh of Bor C, or MELD score greater than 9 or so). If new onset elevation in creatinine is noted, this should prompt an immediate renal consult for further evaluation prior to any anesthetic. Hepatorenal syndrome, can be type 1 or 2. Type 1 is defined by a doubling of serum creatinine to greater than 2.5 mg/dl in less than two weeks, whereas type 2 develops slowly with creatinine rising to greater than 1.5 mg/dl over time. HRS type 1 carries a mortality as high a 80% after two weeks. Unfortunately, the diagnosis is one of exclusion, and there are a myriad of other reasons the cirrhotic patient may have renal dysfunction. In fact, Watt et al. found that only 59% of ARF that was diagnosed as HRS actually fulfilled criteria for the diagnosis, suggesting that HRS is over diagnosed by a large margin. Having a familiarity with the major criteria is helpful and so I've listed them below:
MAJOR CRITERIA:
As desribed above, two phsyicians (the orthopedic surgeon and the GI doc) formulated an independent anesthesia plan and then decided that was best. As consultant anesthesiologists, it is important to effective communicate the need to consider a variety of issues that the anesthesiologist may best suited to consider. The reality is that for hip fracture surgery, spinal anesthesia is a great choice, but not for the reasonas assumed by the two physicians. Spinal anesthesia can impair hepatic artery blood flow as much or more than GETA. Furthermore, these patients are at particular risk for coagulopathy. In patients with low SVR and hypotension, spinal anesthesia may not be tolerated well at all. The reality in our case, was that any anesthesia, spinal or general carried significant risk, but in a patient who did NOT have decompensated liver cirrhosis, it was most prudent to keep the patient and operate as soon as possible for the best possible outcome.
1. D'Amico G, Garcia-Tsao G, Pagliaro L. Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies. J Hepatol. 2006;44:217–231.
2. Park YS et al. Perioperative Risk of Hip Arthroplasty in Patients with Cirrhotic Liver Disease. J Korean Med Sci. 2007 Apr; 22(2): 223–226
4. Northup PG et al. Model for End Stage Liver Disease (MELD) predicts non transplant surgical mortality in patients with cirrhosis. Ann Surg. 2005 Aug; 242(2):244-51 5. Teh SH et al. Risk factors for Mortality after surgery in patients with Cirrhosis. Gastroenterology. 2007 APR; 132(4):1261-9. | |||
| Encephalopathy | None | Grade 1-2 (or precipitant-induced) | Grade 3-4 (or chronic) |
| Ascites | None | Mild/Moderate (diuretic-responsive) | Severe (diuretic-refractory) |
| Bilirubin (mg/dL) | <2 td=""> | 2-3 | greater than 3 |
No comments:
Post a Comment