Page 547 - ACCCN's Critical Care Nursing

524 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

pathophysiology inherent in the end-stage liver failure often experience bibasal collapse and consolidation, and
patient will predispose to varying effects on coagulopathy are prone to infection. Incentive spirometry, chest phys-
and cardiopulmonary, neurological, haemodynamic and iotherapy, early mobilisation and adequate pain relief are
metabolic functions. 299,300 These issues are discussed recommended. 300
below.
Gastrointestinal
Blood loss and coagulopathy Patients with end-stage liver disease often have malnutri-
The major risk during and post-surgery is massive blood tion and bone disease, which may influence post-operative
loss, due to a combination of factors. The surgical process management. Fluid overload and ascites can quite often
itself involves anastomosis of major arteries and veins, mask signs of malnutrition. Early nutrition is imperative
usually in the setting of significant portal hypertension, in the postoperative period. If caloric intake is inade-
predisposing the patient to bleeding and hypovolaemia quate, consultation with a dietitian will assist with enteral
291
during surgery and anastomotic leaks post-surgery. supplementation. Total parenteral nutrition is rarely
Patients with ESLD will also be coagulopathic from required. 304
hepatic synthetic dysfunction, leading to failure of syn-
thetic clotting factors. Correction of coagulopathy with Renal
blood products such as FFP, platelets, cryoprecipitate and Renal dysfunction is a significant posttransplantation
factor VIIa may control minor postoperative bleeding, problem. Risk factors include preexisting renal disease
but if bleeding continues an exploratory laparotomy may or hepatorenal syndrome, intraoperative hypotension,
be required. Conversely, it is not desirable to overcorrect extensive transfusion of blood products, nephrotoxic
coagulopathy, due to the potential for vascular complica- drugs such as cyclosporin and tacrolimus, sepsis, and
305
tions such as hepatic artery thrombosis. Careful monitor- graft dysfunction. Hepatorenal syndrome is reversible
ing is required to identify and manage hypotension, post-transplantation. Patients who are receiving renal
tachycardia, excessive blood loss from drains, falling hae- support such as CRRT usually require continuation of
moglobin, abdominal swelling and oozing from inser- renal support postoperatively for a period of time until
tion sites. Thrombocytopenia is a common postoperative recovery of kidney function is evident (see Chapter 18).
problem, with platelet counts often falling in the first
week post-transplant. If platelet counts are low, a platelet Graft dysfunction and rejection
transfusion may be necessary, especially prior to removal Acute graft rejection was the most challenging obstacle in
of drains, lines, cannulae and sheaths.
the early years of transplantation, but with the develop-
ment of current immunosuppressive therapy, acute
Cardiovascular rejection can be avoided, resulting in improved success
306
Haemodynamic instability in the early postoperative rates of transplantation. Immunosuppressive therapy is
period may be due to hypovolaemia or haemorrhage. commenced intraoperatively with a high-dose steroid
Treatment includes fluid boluses to increase preload and such as methylprednisolone and antibiotic (ticarcillin).
301
the initiation of inotropes may be necessary. The patient Patients are then placed on a triple-therapy regimen
with ESLD may present with a hyperdynamic profile: consisting of steroids such as methylprednisolone and,
high cardiac output, low systemic vascular resistance, later, prednisone, azathioprine and either tacrolimus or
302
and low mean arterial pressure, although this usually cyclosporin. 306,307
reverses one week after transplantation. 300
Allograft dysfunction occurs within 48 hours of trans-
plantation, and is characterised by varying degrees of
Neurological coma, renal failure, worsening coagulopathy, poor bile
The most frequent neurological complications relate to production and marked elevation in the liver enzymes
patients with preexisting encephalopathy and seizures. In (AST, ALT) and worsening acidosis. The cause of allograft
ALF patients, cerebral oedema with raised intracranial dysfunction is not always known; possible causes are
pressure (ICP) is common, and after liver transplanta- injury to the liver, either before or during the donor
tion, cerebral oedema may take up to 48 hours to subside. operation procedure, ischaemic-reperfusion injury or
Therefore, continuation of preoperative measures to graft stenosis. Acute rejection is generally evident in the
reduce ICP are necessary. These include the head of the second week posttransplant, and is generally suspected
bed at 30 degrees, head, neck and body alignment, ensur- with a rise in liver enzymes, a decline in bile quality
ing that endotracheal tapes are not constrictive, aiding (accessible only if a T tube is present), occasional fever
venous return and preventing cerebral congestion, reduc- and tachycardia. 308
ing neurological stimuli and timing activities to prevent
spikes in ICP (see Chapter 17). 302,303 Primary graft non-function is defined as failure of the
graft to function in the first postoperative week. It is
Respiratory manifested by failure to regain consciousness, sustained
elevated transaminases, increasing coagulopathy, acidosis
Preexisting pulmonary complications associated with and poor bile production. Causes include massive
liver disease can affect postoperative recovery and need haemorrhagic necrosis, ischaemia-reperfusion injury and
to be considered when weaning ventilation and main- hepatic artery thrombosis. It may be difficult to distin-
taining adequate oxygenation. Patients posttransplant guish allograft dysfunction, which may recover, from