Monitoring Hepatic Function

The neurological status of the patient should be evaluated and closely monitored; in brief, the conscious level, motor movement, sensory pupil size and reaction to light should be examined. In advanced encephalopathy the pupils may become dilated and react sluggishly to light; if they become dilated and unreactive, brain-stem coning is likely (Steele and Sabol 2009a).

Orientation should be monitored together with concentration span, restlessness, personality and behaviour changes, emotional lability, drowsiness, slurred or slow speech, and disturbances in the sleep pattern. A generalised increase in muscle tone is an early sign of progression of encephalopathy. Spontaneous hyperventilation is common so the respiratory rate should be regularly recorded together with blood gas analysis (Table 9.2).

Table 9.2 Clinical examination of encephalopathy

Reprinted from Oh (1997), with permission from Elsevier Inc.

Cerebral Oedema

Cerebral oedema is a leading, dramatic cause of death in patients with ALF (Stravitz 2008). Patients with acute and hyperacute ALF are more at risk of grade IV hepatic coma and cerebral oedema (Sizer and Wendon 2009). The clinical signs of cerebral oedema, i.e. systemic hypertension, decerebrate posturing and abnormal pupillary reflexes, are generally attributed to brain-stem compression. Cerebral oedema provokes intracranial hypertension that impairs cerebral perfusion pressure.

Cerebral blood flow correlates to arterial pressure and not cardiac output in patients with ALF; strict cardiovascular control is important when pressure-passive cerebral circulation is present in order to maintain continuous and adequate cerebral oxygenation and avoid the development of cerebral hyperaemia and cerebral oedema (Larsen et al. 2000). Close cardiac and haemodynamic monitoring is therefore imperative.

Intracranial pressure (ICP) monitoring is indicated in patients requiring vasopressor agents to maintain adequate cardiac output (Sizer and Wendon 2009).

The benefits of therapeutic prophylactic hypothermia in this population is currently being evaluated in an international multicentre trial (Bernal et al. 2010).

Coagulopathy and Haemorrhaging

Patients with ALF frequently develop severe coagulopathy; the hepatic synthesis of clotting factors is impaired and as a result the clotting times, predominantly prothrombin time and to a lesser extent activated partial thromboplastin ratio (Sizer and Wendon 2009).

The most common site for haemorrhage is the gastrointestinal tract; other sites include the nasopharynx, respiratory tract and skin puncture sites (Stravitz 2008). It is important to monitor for signs of haemorrhage, e.g. in faeces, urine, skin, sputum, endotracheal tube and vomit.

Renal Failure

Renal failure is a common complication of ALF with an incidence of about 50% (Sizer and Wendon 2009). Strict control of fluid balance via renal replacement therapy is indicated in established renal failure (Sizer and Wendon 2009).

Sepsis

Bacterial infection is one of the most common causes of death in patients with ALF and commonly precipitates multiorgan dysfunction syndrome (MODS) (Stravitz 2008). Septic patients are more likely to develop renal failure and gastrointestinal haemorrhaging and have a significantly higher mortality risk than non-septic patients (Sizer and Wendon 2009).

The patient’s vital signs should be closely monitored, and regular cultures of blood, sputum and urine performed (Stravitz 2008).

Ascites may be associated with ALF, spontaneous bacterial peritonitis is a potential complication (Steele and Sabol 2009b).

Metabolic Disturbances

Blood glucose levels should be measured regularly because of the prevalence of hypoglycaemia in these patients. Primary respiratory alkalosis is common in spontaneously breathing patients (see encephalopathy earlier). Impaired hepatic synthesis of urea and hypokalaemia can cause metabolic alkalosis. Electrolyte disturbances are very common.

Scenario

Claire, a 45-year-old woman, was admitted via the emergency department with a history of vomiting and abdominal discomfort. On admission to the ward she was alert but slightly disoriented in time and place. The initial assessment was:

A – airway was patent and she was talking in full sentences

B – respiratory rate was 24/min, SpO₂ was 94%, lung fields clear on auscultation. Oxygen via nasal prongs at 2 l/min applied

C – BP was 95/60, heart rate (HR) 115/min regular, core temperature 35.8°C, peripheries were warm. A urinary catheter was inserted and 100 ml dark urine drained

D – pupils were equal and reacting to light sluggishly. AVPU was A but in view of her disorientation she was started on a Glasgow Coma Scale (GCS) chart

E – Claire’s abdomen was moderately distended with spider naevi evident. She was noted to have significant diffuse bruising with slight jaundice. Claire was also found to have muscle wasting possibly due to poor nutrition

Only gold members can continue reading. Log In or Register to continue