Both Question 1 from the second paper of 2006 and the near-identical Question 1a from the first paper of 2004 asked the candidate to list the problems encountered by a partial hepatectomy patient in the first 48 hours. The older Question 1a also asked about how these complications might be managed. The best reference for an answer to these questions have got to be "Perioperative management of hepatic resection" by Page and Kooby (2012) and "Postoperative manageent of hepatic resection" by Wrighton et al (2012). An excellent alternative is ofered by Thorat and Lee (2013) Unless otherwise stated, these were the main sources for all that follows. Fortunately, this topic can be safely abandoned from the curriculum of the time-poor candidate, as there have been no questions about it for over ten years now.
The use of low CVP during this procedure (0-5mmHg) is a key feature which is unique to liver resection. The whole point is to prevent hepatic venous bleeding. Apparently the difference between this CVP and a more liberal CVP is 200ml vs 1000ml of intraoperative blood loss.
A good summary of the studies is available in Page and Kooby (2012)- their Table 1 compiles the outcomes of contemporary cohorts and trials. In point-form, advantages of a low central venous pressure technique include the following:
A huge ninja-sword cut is usually made, and the patient is usually very sore. An epidural might seem a natural choice, but in fact the sympatholytic effects are counterproductive: by lowering blood pressure the epidural is going to make you give more fluid, and that yields a higher CVP. Page and Kooby (2012) recommend a PCA instead.
This is promoted as an elegant solution to the problem of anticipated blood loss, and is supposed to be a strategy which minimises the loss of red cells. Essentially, the patient donates blood preoperatively, and is then loaded with fluid and albumin, haemodiluting them to a low haematocrit (a Hb target of around 80 g/L is mentioned). The loss of blood is then a loss of very dilute blood, and so fewer RBCs are wasted. Presumably, the banked RBCs are returned to the patient following the end of the procedure. Page and Kooby have only few kind words for this practice.
These are different vascular occlusion manoeuvres. The Pringle Manoeuvre is basically the technique of clamping the entire porta hepatis (apparently, fo no longer than one hour at a time). All other surgical tricks are different variations on this theme, as one can be selective about which vessels one occludes (and one may choose to block inflw, outflow, or both, using external claps, tourniquets, or intravascular balloons).
The anaesthetist should have extubated the patient in recovery or theatre. This is safe, but will have no influence on length of ICU stay (Neelakanta et al, 1997). One may also wish to use NIV if significant atelectasis or ongoing respiratory failure is an issue (reintubation rates will be improved- Narita et al, 2010).
Thorat and Lee recommend the intraoperative low CVP strategy continues during the first 24 hours of ICU stay, and offer 2-5 mmHg as their arbitrary target. While urine output is satisfactory (>0.5ml/kg/hr) no additional fluid is required. One is advised to observe the raised lactate without over-reacting to it, as it does not usually represent a state of global tissue hypoperfusion. The patient will likely be in a state of hyperdynamic distributive shock, which takes a couple of days to settle down.
Beyond saying predictable things about the decreased clearance of benzodiazepines and opiates, one cannot make any useful comments about analgesia and sedation in post-hepatectomy setting. Drugs like hydromorphone and remifentanil are going to be better cleared, but in advanced cirrhosis even the synthesis of nonspecific plasma estherases is impaired, and so the clearance of such drugs will also be delayed. Naturally, one may wish to use a low dose of paracetamol, or to avoid it altogether. For exam purposes, one should use the key phrase "multimodal approach to analgesia".
The pathogenesis of hypophosphatemia after hepatic resection is poorly understood. Apparently, regenerating hepatocytes absorb all the serum phosphate (rates of cell division being high,a nd all the new cells need to make new cytosol, and phosphate is a major intracellular buffer as well as being a key ingredient of phospholipid - so it makes sense that it migh become depleted as a purely structural ingredient). Hypophosphataemia is unpleasant and if left untreated will lead to heart failure and neuromuscular weakness, with predictable effects on ventilator weaning and ICU stay.
When the liver is stressed or damaged, it produces lactate instead of metabolising it. Ergo, the lactate will be raised. The patient will still be conscious, producing urine and with warm extremities, which should put your mind at ease. One might expect the lactate to be a marker of post-op liver dysfunction, but in fact Pagano et al (2015) did not find any value in measuring it post-operatively, as it did not predict whether or not the patient was going to go on to develop significant morbidity, or die. That said,
Patients following liver resection tend to have some combination of lowish blood pressure and ascites. The relevant articles (Wrighton et al, 2012) tend to discuss the use of diuretics and colloids: with one hand, one maintains a circulating volume, and with the other fights ascites.
This issue is covered in detail by Ciuni et al (2011). In brief, the post-hepatic-surgery patient is typically hypercatabolic. The major culprit is the regenerating liver, sucking up all nutritional resources and depleting the body stores of amino acids and carbohydrates. The replenishment of its demand requires attention before the surgery: a well-nourished patient will probably not require any special nutrtional support in the post-op period. If they missed their preadmission clinic appointment and turned up malnoursihed and drunk, your only recourse is to offer supplemental enteral nutrition (by mouth or by nose, their choice). Parenteral nutrition might make you feel better but will have no influence on outcomes (Hotta et al, 2002), whereas enteral nutrition improves wound infection rates (Richter et al, 2006).
Weak evidence also supports the use of branched-chain amino acids, but this is extrapolated from studies performed on non-surgical patients with advanced cirrhosis (Marchesini et al, 2003) and rat studies (Kim et al, 2010). One cannot recommend this with a straight face, but it needs to be mentioned in the exam, because marks.
None of the authors make any firm recommendations regarding the exact increased caloric or protein requirements, merely saying the word "hypercatabolic" over and over again. It is possible that little evidence exists to guid management in this setting. One is tempted to use a trauma-like 2.0-2.5g/kg/day of protein, and a 125-150% increased total caloric goal. The analogy is near-perfect, because the extent of the wound and the tissue loss resemble a wild animal attack or injuries sustained in a machete fight.
One might expect BSL control to go haywaire because a major glucogen storage system has been thrown into the surgical waste bin. However, this is frequently not thecase. Glycogen is aso stored in muscle, and there should be enough liver tissue left to support gluconeogenesis. Still, in patients with advanced cirrhosis one might expect some hypoglycaemia to develop. An again, it is important to mention BSL control in the exam, because reasons. Boxes to tick, etc.
Between day one and day five post liver resection there will be a dip in platelet count and a spike in INR. This is normal, and represents a nadir of synthetic liver function, as well as dilutional coagulopathy. It gets better by itself. There is little consensus among experts regarding the use of prophylactic FFP, but most seem to agree that no correction is required for INR under 2.0, and possibly even higher.