**5.1 Haematological, biochemical and metabolic derangement**

Electrolyte abnormalities are a frequent occurrence in the early post-transplant period. Perioperative hyperkalaemia is often followed by hypokalaemia due to diuretics and polyuria combined with large volume IV fluid replacement. Hypomagnesaemia is exacerbated by the tubular effects of CNI therapy and is associated with an increased risk of post-transplant diabetes [51, 52]. Hypophosphatemia is almost universal as a consequence of elevated FGF23 and PTH levels [53, 54]. To reduce the chance of arrhythmias, intravenous electrolyte replacement should target potassium levels in the normal range (3.5–5 mmol/L) and a serum magnesium >0.4 mmol/L. Hypophosphatemia is not usually associated with adverse clinical sequelae, but if severe (<0.4 mmol/L) can also be managed with intravenous replacement. Many transplant recipients require ongoing oral replacement of potassium, magnesium and occasionally phosphate in the first few weeks post-transplant, although this may be limited by gastrointestinal adverse effects.

Blood tests: Twice daily full blood count and serum biochemistry Alternate day CNI levels Daily capillary glucose levels—if abnormal, manage as diabetes mellitus Post-operative chest radiograph Duplex ultrasound imaging, usually at days 2–4 post-transplant MAG3/DTPA renogram as indicated by clinical progress

#### **Table 6.**

*Common post-operative surveillance investigations.*

Myelosuppression is commonly observed in post-transplant patients receiving immunosuppressive therapy. Myeloid, lymphoid and erythroid lineages can separately be affected in combination. Investigations focus on identification of the underlying cause for the haematological abnormality, and blood films are often helpful.

Post-operative anaemia is observed in around 40% of kidney transplant recipients due to erythropoietin deficiency, pre-transplant anaemia and intra-operative blood loss [55]. Initial management should focus ruling out haemorrhage as discussed in Section 5.2. The administration of an erythropoiesis-stimulating agent may be appropriate in recipients with poor initial graft function [11].

Lymphopenia and neutropenia are also common after transplantation, typically as a consequence of the medication-related bone marrow suppression associated with anti-proliferative agents (mycophenolate and azathioprine), mTOR inhibitors (sirolimus and everolimus) and antiviral agents such as valganciclovir for CMV prophylaxis [56–58]. G-CSF is typically administered if the absolute neutrophil count falls below 1000/μL (1.0 × 109 /L) to try to avoid a severe neutropenia (neutrophil count <500/μL, or < 0.5 × 109 /L), which is associated with a significant risk of severe infections and requires reverse barrier nursing [59]. Alternative causes of neutropenia should also be considered including parvovirus B12 and CMV infection [60].

Thrombocytopenia is comparatively less common, often occurring in conjunction with leukopenia due to bone marrow suppression as previously discussed. More severe thrombocytopenia is a risk factor for bleeding, and platelet transfusion may be necessary if invasive procedures, such as a renal biopsy, are required and the platelet count is <50 × 109 /L [61]. An important consideration, if thrombocytopenia is observed post-transplant, is to look for any other evidence of thrombotic microangiopathy (TMA, **Table 7**) [62]. TMA occurring after transplant may be due to recurrence of primary haemolytic uraemic syndrome, or a de novo problem. Many triggers for de novo TMA post-transplant have been reported, including medication (CNI therapy, particularly in combination with mTOR inhibitors; valacyclovir), and infections (CMV, parvovirus B19) have all been associated with TMA with the potential for graft damage and kidney injury [63–65].

The post-operative stress response, combined with induction corticosteroid and cyclosporine or tacrolimus therapy, can result in significant perioperative hyperglycaemia even in patients who do not have pre-existing diabetes, with a reported incidence as high as 80–90% in some studies [67, 68] with post-transplant diabetes persisting in 10–45% depending on the definition used [69–73]. Hyperglycaemia is also associated with rejection in the perioperative period and in the long term carries adverse metabolic outcomes [74]. It is, therefore, important to monitor capillary glucose levels in all patients after kidney transplantation. Due to the contributions of immunosuppressive medications, and depending on other metabolic risk factors (pre-existing impaired glucose tolerance or diabetes, ethnicity, age and obesity)


**21**

*Perioperative Care for Kidney Transplant Recipients DOI: http://dx.doi.org/10.5772/intechopen.84388*

the scope of this chapter.

ments is essential (Section 5.3).

blood flow indices.

and immune risk, immunotherapy should be individualised [11]. A detailed discussion of the management of post-transplant hyperglycaemia and diabetes is beyond

Perioperative hypotension is common and may reflect inadequate intravascular volume, vasoplegia induced by anaesthetic or analgaesic agents or cardiac dysfunction. Management involves perioperative fluid status optimization with judicious administration of fluid boluses while excluding alternative causes of hypotension including haemorrhage, sepsis and cardiac dysfunction. Recipients with persistent hypotension, despite what appears to be adequate fluid replacement, may require temporary inotropic support. Hypovolaemia, even in the absence of hypotension, increases the risk of delayed graft function resulting in worse graft outcomes [75, 76]. As coronary artery disease is common in patients with ESKD, ruling out ischaemic myocardial damage with ECG review and cardiac enzyme assay measure-

Haemorrhage is common in the early period of kidney transplantation, frequently occurring within 48 h of surgery with a reported incidence of 15% [77]. Apart from hypotension, bleeding may manifest clinically with increasing surgical drain output, pain or swelling at the site of the transplant or a falling haemoglobin on serial blood tests. Risk factors for perioperative bleeding include difficult bench surgery, uraemic platelet dysfunction and administration of antiplatelet agents or heparin (either as thromboprophylaxis or during haemodialysis). In a retrospective analysis, difficult bench surgery was identified as the most significant risk factor for post-operative haemorrhage with a 4-fold increased risk. The use of antiplatelet drugs pre-transplant conferred a 2-fold increased risk. Additionally, dialysis vintage was also a risk factor, and each year on dialysis was associated with a 2% increased bleeding risk [77]. In the early post-operative phase, clinical features suggestive of haemorrhage should prompt urgent review of haematology profile, and consideration of imaging in liaison with the transplant surgeon. Peri-nephric hematomas may be identified on ultrasound, but deep or retroperitoneal haemorrhage may be difficult to identify requiring computed tomography. The development of a peri-nephric haematoma may lead to allograft compression, which if significant, may impair graft perfusion with increased diastolic pressures despite normal, or near normal, arcuate artery

Management of perioperative bleeding requires administration of crystalloid fluids together with judicious transfusion of packed red cells to maintain adequate haemodynamic and haemoglobin targets. Transfusions should be minimised as much as possible, as perioperative blood transfusion leads to recipient sensitization and can increase the likelihood of de novo DSA formation [78]. The decision to proceed to surgical drainage should be individualised, following discussion with the transplant surgeon. The presence of a large haematoma, ongoing haemodynamic instability or features suggesting compression of the allograft, would usually lead to surgical re-exploration. Sepsis should also be considered in the setting of unexplained hypotension. A high index of suspicion for infection should be maintained at all times since transplant recipients may not develop a fever, leukocytosis or raised inflammatory

Due to the significant cardiovascular disease burden and risk associated with chronic kidney disease, cardiovascular complications post-renal transplantation are

markers because of their immunosuppressed state (Section 5.7).

**5.3 Cardiovascular complications**

**5.2 Hypotension: haemorrhage, sepsis and cardiac dysfunction**


#### **Table 7.**

*Features of thrombotic microangiopathy on laboratory tests [66].*

*Perioperative Care for Organ Transplant Recipient*

falls below 1000/μL (1.0 × 109

count <500/μL, or < 0.5 × 109

platelet count is <50 × 109

helpful.

Myelosuppression is commonly observed in post-transplant patients receiving immunosuppressive therapy. Myeloid, lymphoid and erythroid lineages can separately be affected in combination. Investigations focus on identification of the underlying cause for the haematological abnormality, and blood films are often

Post-operative anaemia is observed in around 40% of kidney transplant recipients due to erythropoietin deficiency, pre-transplant anaemia and intra-operative blood loss [55]. Initial management should focus ruling out haemorrhage as discussed in Section 5.2. The administration of an erythropoiesis-stimulating agent

Lymphopenia and neutropenia are also common after transplantation, typically as a consequence of the medication-related bone marrow suppression associated with anti-proliferative agents (mycophenolate and azathioprine), mTOR inhibitors (sirolimus and everolimus) and antiviral agents such as valganciclovir for CMV prophylaxis [56–58]. G-CSF is typically administered if the absolute neutrophil count

infections and requires reverse barrier nursing [59]. Alternative causes of neutropenia should also be considered including parvovirus B12 and CMV infection [60]. Thrombocytopenia is comparatively less common, often occurring in conjunction with leukopenia due to bone marrow suppression as previously discussed. More severe thrombocytopenia is a risk factor for bleeding, and platelet transfusion may be necessary if invasive procedures, such as a renal biopsy, are required and the

is observed post-transplant, is to look for any other evidence of thrombotic microangiopathy (TMA, **Table 7**) [62]. TMA occurring after transplant may be due to recurrence of primary haemolytic uraemic syndrome, or a de novo problem. Many triggers for de novo TMA post-transplant have been reported, including medication (CNI therapy, particularly in combination with mTOR inhibitors; valacyclovir), and infections (CMV, parvovirus B19) have all been associated with TMA with the

The post-operative stress response, combined with induction corticosteroid and cyclosporine or tacrolimus therapy, can result in significant perioperative hyperglycaemia even in patients who do not have pre-existing diabetes, with a reported incidence as high as 80–90% in some studies [67, 68] with post-transplant diabetes persisting in 10–45% depending on the definition used [69–73]. Hyperglycaemia is also associated with rejection in the perioperative period and in the long term carries adverse metabolic outcomes [74]. It is, therefore, important to monitor capillary glucose levels in all patients after kidney transplantation. Due to the contributions of immunosuppressive medications, and depending on other metabolic risk factors (pre-existing impaired glucose tolerance or diabetes, ethnicity, age and obesity)

/L • Microangiopathic haemolytic anaemia (MAHA)—haemoglobin <10 g/dL with evidence of red cell frag-

potential for graft damage and kidney injury [63–65].

• Thrombocytopenia—platelet count <150 × 109

*Features of thrombotic microangiopathy on laboratory tests [66].*

ments on blood film (schistocytes) • Elevated lactate dehydrogenase • Elevated reticulocyte count

• Elevated bilirubin • Reduced haptoglobin /L) to try to avoid a severe neutropenia (neutrophil

/L [61]. An important consideration, if thrombocytopenia

/L), which is associated with a significant risk of severe

may be appropriate in recipients with poor initial graft function [11].

**20**

**Table 7.**

and immune risk, immunotherapy should be individualised [11]. A detailed discussion of the management of post-transplant hyperglycaemia and diabetes is beyond the scope of this chapter.
