Page 336 - ACCCN's Critical Care Nursing

Cardiac Surgery and Transplantation 313

Hyperacute Rejection rejection (grade 1) is rarely treated, and only 20–40% of
Hyperacute rejection is now a rare form of humoral rejec- mild cases progress to moderate rejection (grade 3A),
95,98
tion that occurs minutes to hours after transplantation usually requiring treatment. Grades 3B and 4 rejection
and results from ABO blood group incompatibility or the are always treated, as they represent myocyte necrosis.
92
recipient having preformed, donor-specific antibodies. Cellular rejection is usually treated with higher doses of
ABO blood group and panel reactive screening of anti- corticosteroids, such as ‘pulse’ doses of methylpredniso-
human lymphocyte antigen (anti-HLA) antibodies lone (1–3 g IV over 3 days), and antilymphocyte anti-
preoperatively minimises the possibility of hyperacute body agents (ATG, ATGAM or OKT3). Humoral rejection
rejection, particularly in health care systems where blood is treated with plasmapheresis, high-dose corticosteroids,
that has been prospectively cross-matched is routinely cyclosphosphamide therapy and antilymphocyte anti-
99,100
used. If it occurs, hyperacute rejection leads to organ body therapy. It may be judicious to review the
failure and rapid activation of the complement cascade, patient’s medications during periods of rejection to
producing severe damage to endothelial cells, platelet ensure that drugs capable of reducing cyclosporin or
activation, initiation of the clotting cascade, and extensive tacrolimus serum levels such as certain anticonvulsants
microvascular thrombosis. There is no effective treat- and antibiotics have not been taken. In addition to aug-
78
ment for hyperacute rejection apart from mechanical mentation of immunosuppression therapy, fluid, phar-
circulatory support or interim retransplantation. macological and mechanical therapeutic interventions
are instituted to support cardiac function, depending on
the degree of ventricular dysfunction.
Acute Rejection Immunosuppression Therapy
Acute rejection can be classified as either cellular or
93
humoral. Cellular rejection involves T-cell infiltration In this section, a brief discussion of immunosuppression
of the allograft. Cellular rejection occurs much more therapies and associated nursing implications is pro-
commonly than humoral rejection, but both may occur vided. To prevent rejection of the transplanted organ,
94
simultaneously. Humoral or microvascular rejection is recipients receive a triple-therapy regimen of immuno-
thought to be primarily mediated by antibodies. Humoral suppression agents for the remainder of their life. Triple-
rejection may occur due to the presence of a positive therapy usually consists of corticosteroids (prednisolone
donor-specific cross-match, or in a sensitised recipient or prednisone), a calcineurin antagonist (cyclosporine or
with preformed anti-HLA antibodies. 95 tacrolimus [FK506]) and an antiproliferative cytotoxic
agent (mycophenolate mofetil, azathioprine or sirolimus/
Percutaneous transvenous endomyocardial biopsy is con- rapamycin). 101,102 For heart patients, sirolimus or rapamy-
96
sidered the gold standard for detecting cardiac rejection. cin may become the cytotoxic drug of choice following
Grading of cardiac rejection is noted in Table 12.4. findings of a recent study that demonstrated a lower
97
In humoral rejection, endomyocardial biopsy reveals incidence of cardiac allograft vasculopathy at 6 and 24
increased vascular permeability, microvascular thrombo- months, and lower rejection rates with sirolimus com-
sis, interstitial oedema and haemorrhage, and endothelial pared with azathioprine. 103
78
cell swelling and necrosis. An echocardiogram is also
performed to evaluate systolic cardiac function. Immunosuppression therapy is commenced preopera-
tively or in operating theatre. Maintenance immunosup-
Therapeutic interventions for rejection vary between pression regimen is usually instituted within hours of
centres and are based on the grade of rejection, degree admission to ICU, with each patient’s immunosuppres-
of haemodynamic compromise, clinical findings and sive needs individually assessed. For instance, the
time elapsed since transplantation. Asymptomatic mild administration time for introduction of the selected
immunosuppressive agent(s) may be delayed in patients
with preexisting renal dysfunction. When the administra-
tion of the usual regimen of immunosuppression is
TABLE 12.4 Standardised cardiac biopsy grading 98 delayed, induction therapy with anti-lymphocyte agents
(anti-thymocyte globulin (ATG), ATGAM or OKT3) or
Grade Nomenclature interleukin-2 receptor antagonists (basiliximab, dacli-
0 No rejection zumab) may be used in the immediate postoperative
period. 104,105 Induction therapy may be used in circum-
1 A. Focal (perivascular or interstitial) infiltrate stances of primary allograft failure perioperatively, e.g.
without necrosis
B. Diffuse but sparse infiltrate without necrosis HLA mismatch (rare), or early humoral rejection, or to
allow for a delay in initiating cyclosporine in patients at
2 One focus only with aggressive infiltration and/or risk of renal failure. 106,107 The common drugs used to
focal myocyte damage
suppress the immune system and the nursing implica-
3 A. Multifocal aggressive infiltrate and/or myocyte tions are illustrated in Table 12.5. As highlighted in the
damage table, some immunosuppressive agents are cytotoxic
B. Diffuse inflammatory process with necrosis
(e.g. mycophenolate mofetil), requiring safety measures
4 Diffuse, aggressive, polymorphous process with during preparation, delivery and disposal. Likewise, some
necrosis, with or without any of the following: immunosuppressive agents will be given IV (e.g. azathio-
infiltrate, oedema, haemorrhage, vasculitis
prine) until patients can eat and drink as they cannot be