 1.

relate clinical manifestation of the following conditions to

its
 pathophysiology:
 1.1 acute pancreatitis
 1.2 acute hepatic failure
 2. assess the severity of acute pancreatitis and the related
risk of mortality
 3. state the “range of clinical syndromes” in acute hepatic
failure:
 3.1 hyper-acute
 3.2 acute
 3.3 subacute
 4. explain the complications associated with acute
hepatic failure:
 4.1 encephalopathy
 4.2 coagulopathy
 4.3 metabolic derangement
 4.4 cardiovascular derangement
 4.5 acute kidney injury (hepatorenal syndrome)
 formulate individualized patient care using the
nursing process as a
 framework for the following conditions:
 5.1 acute pancreatitis
 5.2 acute hepatic failure
 It is part of the digestive system and
produces important enzymes and hormones
that help break down foods.
The pancreas has an
endocrine function because it releases
juices directly into the bloodstream, and it
has an exocrine function because it
releases juices into ducts
 Etiology
 Commonest causes:
 1) Biliary stone disease
 2) Alcohol consumption
 3) Drugs
 4) Trauma
 3) Idiopathic
 4) Unknown
The pathogenesis of Acute
Pancreatitis is thought to be due to
premature activation of digestive
enzymes within the acinar cells.
Ordinarily, pancreatic proenzymes
become activated on release within
the duodenum.
Pancreatitis results from early
activation of pancreatic enzymes,
producing autodigestion of the
pancreas and surrounding tissues.
Digestive enzyme release is amplified
as acinar cells lyse, leading to a
vicious cycle of inflammation and
necrosis.
Acute pancreatitis manifests with the
sudden onset of epigastric pain radiating
to the back.
 Eating food worsens pain;
bending forward ameliorates pain.
Abdominal pain lasts for days
and is associated with anorexia, nausea,
and vomiting
 make (something bad or unsatisfactory) better."the
reform did much to ameliorate living
standards”synonyms:improve, make
better, better, make improvements
to, enhance, help,benefit, boost, amend;
 fever,
 tachycardia,
 and hypotension.
 Abdominal examination reveals epigastric
tenderness, with localized guarding and
rebound. Sluggish or absent bowel
sounds indicate coexisting ileus.
 Less frequent findings signal complications,
 including Grey Turner's (flank ecchymosis)
 or Cullen's (umbilical ecchymosis)
 signs suggestive of retroperitoneal hemorrhage,
 a palpable mass suggestive of a pseudocyst,
 and dullness to percussion of lung fields suggestive
of pleural effusion.
 Grey Turner's sign refers to bruising of
the flanks, the part of the body between the last
rib and the top of the hip. The bruising appears as
a blue discoloration, and is a sign of
retroperitoneal hemorrhage, or bleeding behind
the peritoneum, which is a lining of the abdominal
cavity. Grey Turner's sign takes 24–48 hours to
develop, and can predict a severe attack of acute
pancreatitis.
 Grey Turner's sign may be accompanied
by Cullen's sign. Both signs may be indicative of
pancreatic necrosis with retroperitoneal or
intraabdominal bleeding. Grey Turner's sign is
named after British surgeon George Grey Turner.
 Scoring of patient with acute pancreatitis:
 1) alerted to the presence of potentially
severe diseases
 2) comparisons of severity between
patients
 3) potential new treatments and
interventions
 Serum Amylase and Lipase
 - The diagnosis of Acute Pancreatitis is supported
by an elevation of the
 serum amylase and lipase levels in excess of
three times the upper limit of
 normal. The amylase level becomes elevated
within hours of the development of pain and may
remain elevated for 3 to 5 days.
 Liver function tests (LFT)
 - Mild elevations of LFT results
Full blood count
- Leukocytosis
Serum electrolytes, BUN, creatinine,
glucose, cholesterol, and triglycerides
CRP
ABG
Radiography (abdominal X-Ray,
abdominal ultrasound, abdominal CT,
ERCP)
 is a blood test marker for inflammation in the
body. CRP is produced in the liver and its level is
measured by testingthe blood. CRP is classified
as an acute phase reactant, which means that its
levels will rise in response to inflammation.
 This algorithm is based on the practice guidelines
from the American College of
 Gastroenterology
Dynamic contrast-enhanced
computed tomography (CT) provides
the best
means of accurately visualizing the
pancreas and diagnosing pancreatitis
and its local complications. It may
also be used for guiding
percutaneous catheter drainage.
 Following the initial CT scan, additional scanning is only
indicated if the patient’s clinical condition deteriorates,
usually through the development of
 pancreatic necrosis,
 abscess or
 pancreatic pseudocyst,
 haemorrhage, or
 colonic ischemia
 or perforation.

 Ultrasonography in acute pancreatitis is less useful

since visualisation of the gland may be obscured by ‘gas
filled’ bowel.
 Morphine infusion (2-4 mg/h) is still widely used
despite it may cause spasm
 of the sphincter of Oddi and worsen the pain.

 IV Fentanyl 1-2 ug/h may be used as an

alternative.
3. Endoscopic
ERCP represents an alternative
approach to surgery, particularly
for patients
with severe biliary pancreatitis.
 The role of surgery remains a
controversial area in the management of
severe acute pancreatitis. Current
approach is the concept of a conservative,
non-surgical approach.
 The presence of infected pancreatic
necrosis seems to be an undisputed
 indication for urgent surgery.
Indications for surgery in severe acut
pancreatitis:
Stable but persistent necrosis
Deterioration in clinical course
Abdominal Compartment Syndrome
Deterioration in clinical course
 ‘resting the pancreas’, might improve outcome.

 pancreatic secretions by ‘protease inhibitors’, and

somatostatin &

 octreotide,are in widespread use in the hope of

improving the outcome.
Somatostatin and Octreotide:
potent inhibitors of pancreatic
secretion

• Protease Inhibitors: Aprotinin

and gabexate mesilate are
proteolytic
enzyme inhibitors
 Total parenteral nutrition (TPN) in favour of enteral
nutrition (EN) in supporting the
 critically ill.
 Studies suggest that early EN started within 24
hours of admission to ICU, compared with TPN, is
associated with reduced infective
 complications and hospital length of stay.
 protocol ensuring strict glycaemic control is
recommended.
 Problem 1: Fluid Volume deficit related to fluid
sequestration within the
 peritoneum
 Clinical Assessment Findings
 Tachycardia
 MAP < 70 mmHg
 CVP < 7 mmHg
 Capillary refill > 2 secs
 Urine output < 0.5 ml/kg/hour
 Intervention
 1. Monitor hemodynamic status and oxygenation
(blood pressure, heart rate,
 ECG)
 Keep MAP > 70 mmHg
 Observe ECG for myocardial ischemia
 2. Estimate ongoing fluid losses
 Measure all drainage from tubes, catheters and drains
 Evaluate character of all fluid loss
 Colour, odour, presence of particulate matter, fibrin
and clots
 3. Replace volume with prescribed fluids
(crystalloids/colloids)
 Keep MAP > 70 mmHg
 CVP > 7 mmHg
 Capillary refill < 2 secs
 4. Measure urine output continuously
 Keep Urine output > 0.5 ml/kg/hr
Problem 2 : Pain related to injury
to pancreatic tissue and
surrounding tissue
Clinical Assessment Findings
Patient discomfort evidenced by
pain score
Tachycardia
Irregular respiration
 Intervention
 1. Position patient to optimize comfort
 2. Reduce anxiety that may contribute to pain relief
 Provide reassurance
 3. Administer IV analgo-sedation
 Provide Midazolam/Morphine infusion 1-2mg/hour
 4. Monitor hemodynamic and respiration
 5. Assess level of pain by using Pain Score
 Report if patient is persistently in pain. Dose of
analgesia need to be
 adjusted accordingly
 Clinical Assessment Findings
 Weight loss
 Intervention
 1. Assess nutritional status
 Body weight
 2. Nutritional management
 Collaborate with dietitian and pharmacist to estimate
patients’ nutritional needs.
 Administer enteral feeding if tolerated.
 Administer Total Parenteral Nutrition if enteral
feeding cannot be established.
 In the majority of AHF, there is widespread
hepatocellular necrosis beginning in
 the centrizonal distribution and progressing
towards portal tracts. The degree of
 parenchymal inflammation is variable and is
proportional to duration of disease.
 Acute hepatic failure (AHF) is a complex multi
systemic illness that evolves after
 significant liver insult. It is a heterogeneous
condition incorporating a range of
 clinical syndromes.
“Range of Clinical Syndromes” In Acute
Hepatic Failure
Acute hepatic failure (AHF) is a complex
multi-systemic illness that evolves after
significant liver insult. It is a
heterogeneous condition incorporating a
range of
clinical syndromes. Definitions according
to O’ Grady:-
 1. Hyper-acute
 - the onset of encephalopathy is within 7
days of the development of jaundice
 2. Acute
 - encephalopathy develops 8-28 days
after the onset of jaundice
 3. Sub-acute
 - encephalopathy develops 4-26 weeks
after the onset of jaundice
1. Encephalopathy
The spectrum extends from mild
confusion progressing to deep
coma,cerebral edema and raised
intracranial hypertension.
 Coagulopathy is another cardinal feature of AHF. The
liver has the central role in synthesis of almost all
coagulation factors and some inhibitors of coagulation
and fibrinolysis. Hepatocellular necrosis leads to
impaired synthesis of many coagulation factors and
their inhibitors. The former produces a prolongation in
prothrombin time which is widely used to monitor
severity of hepatic injury. There is significant platelet
dysfunction (with both
 quantitative and qualitative platelet defects).
Progressive thrombocytopenia with loss of larger and
more active platelet is almost universal.
 Thrombocytopenia with or without DIC increases the
risk of intracerebral
 bleeding.
 Hypernatremia is an almost universal finding due
to water retention and a shift in intracellular
sodium transport from inhibition of Na/K ATPase.
 Hypoglycemia (due to depleted hepatic glycogen
store and yperinsulinaemia), hypokalemia,
hypophosphatemia and metabolic alkalosis are
often present, independent of renal function.
Lactic acidosis occurs predominantly in
paracetamol overdose.
 Patient with AHF develop hyper-dynamic circulation, with
peripheral vasodilatation and central volume depletion.
This will leads to hypotension
 and may initially respond to volume replacement. There is
a compensatory increase in cardiac output. Hypotension
that does not respond to volume will
 require some form of invasive hemodynamic monitoring
and frequently institution of vasopressor agents. The
requirement for vasopressor agents
 should raise the possibility of adrenal dysfunction.
Hydrocortisone replacement therapy should be considered.
 Renal failure is common, present in more than 50% of
AHF patients, either due to original insult such as
paracetamol resulting in acute tubular necrosis or from
hyperdynamic circulation leading to ‘hepatorenal
syndrome’ or functional renal failure. Because of
impaired production of urea, blood urea does not
represent degree of renal impairment. Established
renal failure requires the institution of renal
replacement therapy (RRT). The hemodynamic
instability and associated cerebral complications have
resulted in the application of continuous modes of
RRT rather than intermittent hemodialysis.
 Management of ALF patients in ICU requires an
experienced multidisciplinary team.

 Patients with stage I HE experience changes in

behavior, with minimal changes in their level of
consciousness, and may be initially managed in a step
-down or ward setting. On the other hand, patients
with drowsiness, asterixis, and any
 degree of disorientation (stage II HE) are at a high risk
of decompensation and warrant ICU admission.
Patients with more severe neurologic impairment
(stages III – IV HE) require intubation and mechanical
ventilation.
 a) Ammonia-lowering therapy with lactulose has
been the mainstay of treatment
 for HE. A nasogastric tube may be used to
administer the frequent doses of
 this medication. With lactulose therapy, the
potential side effect of colonic
 distention should be taken into consideration.
 b) Cerebral edema and ICH can lead to death from cerebral
herniation.
 Recommended management includes intubation, sedation, head-of-
bed
 elevation to at least 30 degrees, and efforts to minimize
interventions and
 stimuli that result in increased ICP. Prophylactic dosing of
antiepileptic
 medications has not been shown to improve outcomes. Intravenous
mannitol
 at a dose of 1 g/kg body weight (dose range 0.25–2 g/kg) is a first-
line
 therapy that may be used. Hyperventilation to reduce PaCO2 to
25–30 mmHg has been used as a short term solution to decrease
cerebral blood flow and lower ICP.
 c) Infection has consistently remained the number
one cause of death in ALF
 patients. Frequent surveillance of blood, urine,
and sputum cultures has been
 shown to be useful and can direct therapy.
Prophylactic antibiotics have been
 shown to reduce infection rates, though their use
has not been directly linked
 to improved outcomes.
 d) The circulatory disturbance in ALF is
characterized by decreased systemic
 vascular resistance and elevated cardiac output.
Management consists of
 intravenous fluid resuscitation and vasopressors
guided by invasive
 hemodynamic monitoring.
e) Adrenal insufficiency is commonly
seen in ALF. The presence of
persistent
hypotension despite volume
resuscitation and vasopressors will
require
empiric treatment with intravenous
steroids.
 f) Acute kidney injury (AKI) is common in ALF. Renal
failure often coexists with
 a variety of metabolic derangements, including lactic
acidosis, hyponatremia,
 hypophosphatemia, and, often profound hypoglycemia
requiring continuous
 glucose infusion. The decision of when to begin renal
replacement therapy
 (RRT) has been a subject of debate. There is
agreement that when an acute
 indication for RRT exists, continuous RRT, rather than
intermittent
 hemodialysis, is preferred to minimize cardiovascular
disturbances and
 increased ICPs.
 g) The risk of bleeding in ALF patient is increased in the
setting of AKI and ICH.
 They often have markedly elevated prothrombin times or
INRs, as well as
 thrombocytopenia, though these measures do not always
correlate to
 increased rates of bleeding. Correction of coagulopathy
with fresh frozen
 plasma or thrombocytopenia with platelet transfusion is not
indicated unless
 an invasive procedure is planned. Vitamin K should be
administered to
 facilitate synthesis of prothrombin and coagulation factor if
liver is functional.
 h) Nutrition is another consideration in ALF
patients, with electrolyte and vitamin
 replacement being important, as well as early
initiation of enteral nutrition.
 Protein restriction is not indicated, and 1g/kg per
day of protein is
 recommended. Parenteral nutrition may be
needed if enteral nutrition is
 contraindicated.
 Nursing Care of Patients with Acute Hepatic
Failure
 Problem 1: Ineffective cerebral tissue perfusion
related to hepatic
 encephalopathy
 Clinical assessment findings
 - Worsening level of consciousness
 Interventions
 1. Administer oxygen to improve cerebral
oxygenation
 2. Intubate and ventilate if GCS < 8 or inability to
maintain adequate airway
 3. Hyperventilation and intermittent Mannitol
boluses as temporary measures to
 reduce ICP and increase cerebral perfusion
pressure
 4. Monitor vital signs and hemodynamic
parameters
 5. Monitor neurological status for changes in
mentation or level of consciousness
 6. Monitor peripheral pulses
 7. Monitor laboratory data: electrolytes,
coagulation profile, renal profile, liver
 function, glycemia control
 8. Administer lactulose to reduce ammonia levels
 9. Use sedation to reduce stimuli for increasing
ICP or reduce cerebral
 metabolism such as benzodiapines, propofol and
opioids.
 Problem 2: Risk of bleeding related to coagulopathy
 Clinical assessment findings
 - Presence of petechiae, hematoma or bruising
 Interventions
 1. Monitor the presence of blood in body secretions eg
stool, urine and NG aspirate
 2. Observe for bleeding from puncture sites
 3. Monitor vital sign and hemodynamic parameters that
could indicate loss of circulating blood volume
 4. Insert NG tube gently to prevent from bleeding
 5. Administer Vitamin K that facilitates synthesis of
coagulation factor