**12. Cardiac complications after LT**

Cirrhotic cardiomyopathy (CCM) is defined as cardiac dysfunction in patients with cirrhosis characterized by a blunted contractile responsiveness to stress and/ or diastolic dysfunction and electrophysiological abnormalities in the absence of known cardiac disease [96]. Diagnostic features include a reduced ejection

fraction (EF), an E/A ratio < 1, and electrocardiographic abnormalities such as a prolonged QTc interval. Diagnostic approaches involve transthoracic ultrasound, dobutamine stress echocardiography (DSE), as well as cardiac magnetic resonance (CMR). The concept of "ventriculo-arterial coupling" (VAC) has recently been suggested as a means of assessing cardiac function in ESLD. The VAC (ratio of ventricular elastance to arterial elastance) is measured conventionally by ultrasound and has been correlated with prognosis. Moreover, cardiac biomarkers such as troponin and brain natriuretic peptide (BNP) are deemed early markers [97].

It is difficult to define the exact impact of CCM due to the fact that its clinical course is usually silent, especially in early stages, due to the profound vasodilatation in cirrhosis and offloading of the left ventricle. It only becomes apparent in conditions of stress and increased afterload. LT is a cause of significant cardiovascular stress since there are marked variations in preload and afterload, cardiac workload increases and the existing underlying cardiac dysfunction may become overt heart failure during LT or several days postoperatively. Complete recovery has been recorded at 6 months [98].

Cardiac dysfunction and pulmonary edema are encountered in almost half of the patients within a week after LT. They have been identified as the third most important cause of mortality during the first year following the surgery. High MELD score and AKI have been considered as risk factors. Early diagnosis can prevent acute onset or deterioration of heart failure. An empirical and supportive therapeutic approach is applied which includes optimization of volume status and cardiac monitoring via echo and/or PAC [99, 100].

Prevalence of coronary artery disease (CAD) in cirrhosis reaches 5–26% and has been associated with poor prognosis. It has been correlated with a number of cardiac adverse events: myocardial infraction, arrhythmias, and cardiac death. LT can be postponed in cases with known CAD for medical optimization and/or revascularization [99, 100].

## **13. Neurological complications**

Neurological complications (NC) are still common after LT with a 15–30% incidence rate. In recipients from living donors, this percentage does not exceed 20% [101, 102]. Major neurologic complications immediately postoperatively include alterations of consciousness, seizures, hepatic encephalopathy, CNI neurotoxicity, cerebrovascular complications, central nervous system infections, and central pontine myelinolysis (CPM) [103]. They can delay recovery and make immunosuppression and patient management difficult. Rapid patient recovery requires daily evaluation of mental status and neurological assessment in the ICU.

Immunosuppression-related neurotoxicity can range from headaches and convulsions to posterior reversible encephalopathy (PRES). Immunosuppressants have the potential to reduce the seizure threshold that is enhanced by electrolytic disorders mainly hypomagnesaemia and hypophosphatemia. CNIs are mainly implicated while incidents of PRES have been reported even in treatment with sirolimus. The treatment is conservative involving reduction of dosage and/or interchange with CNI-sparing regimens. Neurotoxicity of corticosteroids can be manifested either in the form of convulsions or myopathy and behavioral disorders [103].

Post-transplant encephalopathy is responsible for 12% of NC. It relates closely to metabolic disorders, CNS infections and/or septic encephalopathy, cerebrovascular events, history of severe encephalopathy, and graft dysfunction [78]. Seizures are one of the most common postoperative neurological consequences and may be the effect of various factors, mainly drug toxicity and metabolic disorders. Correction of underlying causes and administration of anti-convulsive medicines are the appropriate treatment.

**203**

**Table 3.**

2.9%

1–2%

0.64%

5%

2%

**Table 4.**

*Management of Patients with Liver Transplantation in ICU*

Na serum values to 8–10 mEq/L per day [104, 105].

**15. Postoperative surgical complications**

Abdominal bleeding Anastomosis site

Biliary Complications Biloma, Hemobilia

**15.1 Early surgical complications**

*Immediate surgical complications after LT.*

Hepatic artery thrombosis (HAT)

Hepatic artery stenosis (HAS)

Hepatic artery rupture (HAR)

Portal vein thrombosis (PVT)

Portal vein stenosis (PVS)

*Vascular complications after LT.*

Central pontine myelinolysis (CPM) represents a serious complication, with a low incidence of approximately 1–3.5% that may affect the postoperative course of patients. It has been associated with large fluid shift and rapid correction of prolonged hyponatremia. The indicated treatment is supportive and requires careful correction of severe hyponatremia (serum Na <125 mEq/L), which is encountered in approximately 17% of patients with ESLD, using sodium chloride and adjusting

Ischemia-reperfusion injury is related with the degree of transaminitis and primary and/or delayed graft dysfunction. Mitochondria are more prone to I/R injuries with subsequent alterations that can lead to dysfunction or even to necrosis of hepatocytes following LT. Alternatively, machine reperfusion has been proposed to preserve the donor organ. It promises to restore energy balance, extend preservation time while offering the ability to "test" the organ performance [106, 107].

In the early postoperative period, according to Parikh et al., 79.3% of patients are present with at least one complication with 62.8% of the recipients suffering severe

Re-operation

HIDA

or

ERCP, PTC, MRCP EUS-guided approach

Digital Cholagiography

Surgical re-intervention

Emergent revascularization (endovascular or surgical) or re-LT

Endovascular intervention or surgical HA revision

Emergent surgical hemostasis

Endovascular intervention

Endovascular intervention or re-LT

and surgical repair

Surgical revision

**Complications Diagnosis-treatment Therapeutic approach**

Anastomosis necrosis Anastomotic stricture

Graft surface Diffusion bleeding

Bile leaks

**Vascular complications Diagnosis Treatment**

DUS, CT Angiography

DUS, CT Angiography

Angiography None in emergency

Venography

Venography

DUS, CT (portal phase)

DUS, CT (portal phase)

*DOI: http://dx.doi.org/10.5772/intechopen.89435*

**14. Ischemia reperfusion injury**

*Management of Patients with Liver Transplantation in ICU DOI: http://dx.doi.org/10.5772/intechopen.89435*

Central pontine myelinolysis (CPM) represents a serious complication, with a low incidence of approximately 1–3.5% that may affect the postoperative course of patients. It has been associated with large fluid shift and rapid correction of prolonged hyponatremia. The indicated treatment is supportive and requires careful correction of severe hyponatremia (serum Na <125 mEq/L), which is encountered in approximately 17% of patients with ESLD, using sodium chloride and adjusting Na serum values to 8–10 mEq/L per day [104, 105].

### **14. Ischemia reperfusion injury**

*Liver Disease and Surgery*

fraction (EF), an E/A ratio < 1, and electrocardiographic abnormalities such as a prolonged QTc interval. Diagnostic approaches involve transthoracic ultrasound, dobutamine stress echocardiography (DSE), as well as cardiac magnetic resonance (CMR). The concept of "ventriculo-arterial coupling" (VAC) has recently been suggested as a means of assessing cardiac function in ESLD. The VAC (ratio of ventricular elastance to arterial elastance) is measured conventionally by ultrasound and has been correlated with prognosis. Moreover, cardiac biomarkers such as troponin

It is difficult to define the exact impact of CCM due to the fact that its clinical course is usually silent, especially in early stages, due to the profound vasodilatation in cirrhosis and offloading of the left ventricle. It only becomes apparent in conditions of stress and increased afterload. LT is a cause of significant cardiovascular stress since there are marked variations in preload and afterload, cardiac workload increases and the existing underlying cardiac dysfunction may become overt heart failure during LT or several days postoperatively. Complete recovery has been recorded at 6 months [98]. Cardiac dysfunction and pulmonary edema are encountered in almost half of the patients within a week after LT. They have been identified as the third most important cause of mortality during the first year following the surgery. High MELD score and AKI have been considered as risk factors. Early diagnosis can prevent acute onset or deterioration of heart failure. An empirical and supportive therapeutic approach is applied which includes optimization of volume status and

Prevalence of coronary artery disease (CAD) in cirrhosis reaches 5–26% and has been associated with poor prognosis. It has been correlated with a number of cardiac adverse events: myocardial infraction, arrhythmias, and cardiac death. LT can be postponed in cases with known CAD for medical optimization and/or

Neurological complications (NC) are still common after LT with a 15–30% incidence rate. In recipients from living donors, this percentage does not exceed 20% [101, 102]. Major neurologic complications immediately postoperatively include alterations of consciousness, seizures, hepatic encephalopathy, CNI neurotoxicity, cerebrovascular complications, central nervous system infections, and central pontine myelinolysis (CPM) [103]. They can delay recovery and make immunosuppression and patient management difficult. Rapid patient recovery requires daily

Immunosuppression-related neurotoxicity can range from headaches and convulsions to posterior reversible encephalopathy (PRES). Immunosuppressants have the potential to reduce the seizure threshold that is enhanced by electrolytic disorders mainly hypomagnesaemia and hypophosphatemia. CNIs are mainly implicated while incidents of PRES have been reported even in treatment with sirolimus. The treatment is conservative involving reduction of dosage and/or interchange with CNI-sparing regimens. Neurotoxicity of corticosteroids can be manifested either in

Post-transplant encephalopathy is responsible for 12% of NC. It relates closely to metabolic disorders, CNS infections and/or septic encephalopathy, cerebrovascular events, history of severe encephalopathy, and graft dysfunction [78]. Seizures are one of the most common postoperative neurological consequences and may be the effect of various factors, mainly drug toxicity and metabolic disorders. Correction of underlying causes and administration of anti-convulsive medicines are the appropriate treatment.

evaluation of mental status and neurological assessment in the ICU.

the form of convulsions or myopathy and behavioral disorders [103].

and brain natriuretic peptide (BNP) are deemed early markers [97].

cardiac monitoring via echo and/or PAC [99, 100].

revascularization [99, 100].

**13. Neurological complications**

**202**

Ischemia-reperfusion injury is related with the degree of transaminitis and primary and/or delayed graft dysfunction. Mitochondria are more prone to I/R injuries with subsequent alterations that can lead to dysfunction or even to necrosis of hepatocytes following LT. Alternatively, machine reperfusion has been proposed to preserve the donor organ. It promises to restore energy balance, extend preservation time while offering the ability to "test" the organ performance [106, 107].
