Page 542 - ACCCN's Critical Care Nursing

Gastrointestinal, Liver and Nutritional Alterations 519

circulation (low systemic vascular resistance and high
265
Practice tip cardiac output) seen in liver failure. Other factors, such
as pleural effusions or severe ascites, may impinge on
Avoid using lactate- or citrate-buffered substitution/dialysis ventilation.
fluid for renal replacement therapy in patients with liver dys-
function, as they will be unable to metabolise the lactate or Haemodynamic Instability, Susceptibility
citrate and will develop an increasing metabolic acidosis. to Infection, Coagulopathy and
Metabolic Derangement
Varices and Variceal Bleeding The hyperdynamic, low vascular resistance picture, similar
to that associated with sepsis, is seen in liver dysfunction.
The development of varices and variceal bleeding arises This probably results from the production of vasodilator
from portal hypertension. This manifests when blood substances (nitric oxide) from the inflammatory response
flowing from an area of high pressure (i.e. the cirrhotic of the injured liver cells. 234 Sepsis may also be a complica-
liver) to areas of lower pressure (i.e. the collateral circula- tion of liver dysfunction because of the failure of the liver
tion, involving veins of the oesophagus, spleen, intestines to produce acute-phase proteins and the impaired func-
and stomach), causes the tiny, thin-walled vessels to tion of Kupffer cells. 237
become engorged and dilated, forming varices that are
vulnerable to gastric secretions, resulting in rupture and Hepatocyte damage leads to a decreased production of
haemorrhage. 241,264 Variceal haemorrhage is a major cause the majority of clotting factors and, therefore, haemosta-
of acute decompensation and a reason for admission to sis. Therefore, the risk of bleeding is elevated. 266 Disor-
the ICU. It is an acute clinical event characterised by dered metabolic function and failure of synthetic function
severe gastrointestinal haemorrhage presenting as hae- can manifest as unstable blood glucose levels.
matemesis, with or without melaena, and haemodynamic
instability (tachycardia and hypotension). 241,264 Practice tip

Patients in ALF or AoCLF are at risk of hypoglycaemia, and
Practice tip blood glucose levels should be measured routinely.
Coagulation state and the risk of trauma to varices should be
carefully considered before insertion of nasogastric or orogas- NURSING PRACTICE
tric tubes, or suctioning of the upper airway. Trauma may result The management of patients with liver dysfunction is
in epistaxis with significant bleeding or variceal bleeding. complex and involves multisystem organ support, and
as such requires a multidisciplinary and collaborative
Ascites approach to patient care.
Ascites is usually present in the patients with chronic liver INDEPENDENT PRACTICE
disease. In the ICU setting it becomes an issue when Early signs of the patient presenting with ALF are malaise,
abdominal pressures rise, resulting in reduced cardiac loss of appetite, fatigue, nausea, jaundice, bruising, bleed-
output due to decreased venous return and renal impair- ing, inflamed/enlarged liver, possibly epigastric and right-
ment. Pressure on the diaphragm causes loss of lung upper-quadrant pain, high or low blood glucose levels
volume, resulting in increased work of breathing and (which require monitoring, at least every 4 hours; patients
compromised oxygenation. may require insulin infusion or 10–50% dextrose infu-
sion), deranged liver function tests (LFTs) and fluctuating
GCS due to cerebral oedema. 237 If acute liver failure is
Practice tip suspected, admission to an ICU is recommended to
Patients with AoCLF may develop ascites, causing a rise in intra- monitor for further deterioration, and provide supportive
abdominal pressure (IAP). Raised IAP has negative effects on management and airway protection. The patient present-
work of breathing, cardiac preload and intra-abdominal organ ing with AoCLF will have similar symptoms but will
perfusion. IAP should be measured (see Chapter 23). present with other unique characteristics. Cirrhosis and
portal hypertension will often lead to oesophageal and
gastric varices, ascites, hepatorenal and hepatopulmonary
Respiratory Compromise syndrome, malnutrition, bone disease, sepsis, palmar ery-
Patients with liver failure may have poor oxygen exchange, thema, spider naevi and feminisation in males. 267
fluctuating GCS that requires intubation for airway pro- If liver failure is suspected, investigating ingestion of
tection and hepatopulmonary syndrome (HPS). HPS is hepatotoxic substances (paracetamol, steroids, ethanol),
found in 15–20% of patients with cirrhosis. 265 It is defined oral or intravenous recreational drug use, and any recent
as pulmonary microvascular dilation resulting in impaired travel (viral infections) is required.
oxygenation, and it is generally assumed that vascular
production of vasodilators, specifically nitric oxide, Neurological Considerations
underlies the vasodilation in HPS. It has also been Cerebral oedema is present in 80% of patients with
hypothesised that the mechanisms that trigger HPS are grade IV encephalopathy and is the leading cause of
the same as those that result in the hyperdynamic death due to brain herniation. 268 Patients with cerebral