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