| Upper Gastrointestinal Bleeding Posted: 23 Sep 2010 07:14 PM PDT 
Upper gastrointestinal bleeding is characterized by the sudden onset of bleeding from the GI tract at a site (or sites) proximal to the ligament of Treitz. Most upper GI bleeds are a direct result of peptic ulcer erosion, stress related- mucosal disease, that may evidence as superficial erosive gastric lesion to frank ulcerations, erosive gastritis (secondary to use or abuse of NSAIDs, oral corticosteroids, or alcohol) or esophageal varices (secondary to hepatic failure). In addition to these, Mallory-Weiss tears can cause gastroesophageal bleeding as a result of severe retching and vomiting, but the bleeding tends to be less severe than in other types. Hospitalized critically ill patients are at heightened risk for stress related mucosal disease, particularly if they are intubated and mechanically ventilated and/or evidencing coagulopathies. Signs and Symptoms - Melena and hematemesis
- Pain
- Hypovolemic shock
Physical Examination Vital signs - BP < 90 mm Hg
- HR > 100 beats/min
- RR: tachycardia
- Temperature: maybe elevated
Other - Hematemesis
- Melena
- Bloody stool with fetid odor
- Coffee ground gastric aspirate
Skin - Pale, diaphoretic
- Cool, clammy
- Jaundice
Cardiovascular - Weak, thready pulse
- Capillary refill > 3 sec
Abdominal - Maybe tender with guarding
- Bowel sounds hyperactive or absent
Acute Care Patient Management Nursing Diagnosis: Deficient fluid volume related to blood loss from hemorrhage. Outcome Criteria - Patient alert and oriented
- Skin, pink, warm, and dry
- CVP 2 to 6 mm Hg
- PAS 15 TO 30 mm Hg
- PAD 5 to 15 mm Hg
- BP 90 to 120 mm Hg
- MAP 70 to 105 mm Hg
- HR 60 to 100 beats/min
- Urine output 30 ml/hr
Patient Monitoring - Obtain pulmonary artery pressure, central venous pressure and blood pressure every 15 minutes during acute episodes to evaluate fluid needs and the patient's response to therapy.
- Monitor fluid volume status. Measure intake and output hourly to evaluate renal perfusion.
- Measure blood loss if possible.
- Continuously monitor ECG for dysrythmias and myocardial ischemia.
Patient Assessment - Assess patient for increases restlessness, apprehension or altered consciousness, which may indicate decreased cerebral perfusion.
- Assess hydration status.
- Be alert for recurrence of bleedings.
Diagnostic Assessment - Review Hgb and Hct levels to determine the effectiveness of treatment or worsening of the patient's condition.
- Review clotting factors and serum calcium levels if multiple transfusions have been give.
- Review serial BUN levels.
- Review serial ABGs to evaluate oxygenation and acid-base status.
- Review the result of endoscopic evaluation.
Patient Management - Maintain a patent airway. Administer supplemental oxygen as ordered.
- Administer colloids as ordered to restore intravascular volume.
- Type and crossmatch for anticipated blood products.
- Evacuate stomach contents with nasogastric tube and initiate lavages with room temperature water or saline to clear blood clots from the stomach.
- Continue to monitor the patient closely once stabilized.
- Vitamin K or fresh-frozen plasma (FFP) may be ordered to correct coagulation deficiencies.
- Explain all procedures and tests to the patient to help alleviate anxiety and decreased tissue oxygen demands.
Related posts: - Hypovolemic Shock Patient Care and Monitoring
- Hypovolemic Shock
- Hepatic Failure
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| Hepatic Failure Posted: 23 Sep 2010 07:07 PM PDT 
Hepatic failure can result from acute liver injury, causing acute liver failure (ALF) or fulminant hepatic failure (FHF), or progressive chronic liver disease such as cirrhosis. An alteration in hepatocyte functioning affects the liver metabolism, detoxification process, protein synthesis, manufacture of clotting factors, and preservation of immunocompetence. FHF occurs when severe hepatic injury results in encephalopathy and severe coagulopathy within 28 days of the onset of symptoms in patients without a history of chronic liver disease. Liver transplant is the only viable treatment option for patient with FHF. The most commonly identified cause of FHF is drug induced, with acetaminophen the most common culprit, followed by viral hepatitis. Other causes include infection (cytomegalovirus [CMV], adenovirus), metabolic disorders and severe ischemic insult or shock. Signs and Symptoms - Manifestation depends on the complications associated with the liver dysfunction.
- Patient behavior may range from agitation to frank coma.
- Evidence of GI bleeding, renal failure, or respiratory distress may also be present.
- The initial manifestation in FHF is commonly bleeding from coagulopathy.
Physical Examination Vital signs - BP: < 90 mm Hg (with shock)
- HR: > 120 beats/min (with shock)
- Temperature may be mildly elevated
- RR: tachypnea initially progressing to respiratory depression associated with encephalopathy.
Neurologic - Mildly confused to coma
- Personality changes
- Asterixis
Pulmonary - Crackles
- Labored respirations
Gastrointestinal - Hematemesis and melena
- Ascites
- Hepatomegaly may be present
- Splenomegaly may be present
- Factor hepaticus
- Diarrhea
Skin - Jaundice
- Ecchymosis and petechiae
- Pruritus
- Edema
Acute Care Patient Management Nursing Diagnosis: Deficient fluid volume related to ascites secondary to hypoalbumineia, bleeding secondary to decreased clotting factors or variceal hemorrhage, and diuretic therapy. Outcome Criteria - BP 90 TO 120 mm Hg
- Central venous pressure 2 to 6 mm Hg
- Serum albumin 3.5 to 5 mg/dl
- Platelet count >50,000/mm3
- Urine output 30 ml/hr
- Serum sodium 135 to 145 mEq/L
- Serum potassium 3.5 to 5 mEq/L
- Intake approximates output
Patient Monitoring - Obtain pulmonary artery pressure, central venous pressure, and blood pressure until the patient's condition is stable, then hourly.
- Continuously monitor ECG for lethal dysrhythmias that may result from electrolyte and acid-base imbalances.
- Monitor fluid volume status. Measure intake and output hourly.
Patient Assessment - Assess hydration status. Note skin turgor on inner thigh or forehead, condition of buccal memranes, and development of edema and crackles.
- Assess for signs and symptoms of bleeding.
- Measure abdominal girth once each shift to determine progression of ascites.
- Assess respiratory status.
Diagnostic Assessment - Review serial serum ammonia, albumin, bilirubin, platelet count, PT, PTT and ALT to evaluate hepatic function.
- Review serial serum electrolytes.
- Review urine electrolyte, BUN, and creatinine to evaluate renal function.
Patient Management - Administer intravenous crystalloids as ordered.
- Administer potassium as ordered. Validate adequate urine output before potassium administration.
- Sodium restriction of 0.5 g/day and fluid restriction to 1000 ml/day may be ordered.
- Vitamin K or fresh frozen plasma (FFP) may be required to promote the clotting process.
- Institute bleeding precautions. Avoid razor blades and use soft-bristled toothbrushes.
- Paracentesis may be performed if abdominal distention is severe.
- Prepare the patient and family for liver transplant, as indicated.
Related posts: - Upper Gastrointestinal Bleeding
- Acute Renal Failure
- Hypovolemic Shock
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| Sudden Cardiac Death Posted: 23 Sep 2010 07:00 PM PDT 
Sudden cardiac death (SCD) is unexpected cardiopulmonary collapse. SCD can occur as a primary manifestation of ischemic heart disease. Risk factors mirror the risk factors for coronary artery disease (CAD); cigarette smoking, hyperlipidemia, hypertension, diabetes, obesity, stress, and a positive family history of cardiovascular disease. Men, especially those older than 50 years, and postmenstrual women are susceptible. Additional risk factors include patients who: - Has known sudden cardiac death survivors.
- Had an acute MI within the past 12 months.
- Have cardiomyopathies that have demonstrated left ventricular ejection fractions <40%,
- Had prolonged QT intervals.
Signs and Symptoms - A previously normal-appearing adult will suddenly collapse with cardiopulmonary arrest not associated with accidental or traumatic causes.
- There are commonly no prodromal symptoms, although there may be a brief period of anxiousness or chest discomfort.
Physical Examination - Full cardiopulmonary arrest
- Pulselessness
- No respirations
Acute Care Patient Management Nursing Diagnosis: Decreased cardiac output related to electrophysiologic instability after resuscitation. Outcome Criteria - Patient alert and oriented
- Skin warm and dry
- HR 60 to 100 beats/min
- Absence of lethal dysrhythmias
- BP 90 to 120 mm Hg
- Mean arterial pressure 70 to 105 mm Hg
- Urine output 30 ml/ hr
Patient Monitoring 1. Monitor in the lead appropriate for ischemia or dysrhythmia identification. 2. Analyze ECG rhythm strip at least every 4 hours and note rate, rhythm. 3. Obtain pulse arterial pressures and central venous pressure hourly or more frequently if titrating pharmacologic agents. 4. Monitor arterial oxygen delivery and oxygen consumption as indicators of tissue perfusion. 5. Monitor blood pressure hourly. 6. Monitor hourly urine output to evaluate effects of decreased cardiac output and pharmacologic intervention. Diagnostic Assessment - Review serial 12 lead ECGs and cardiac enzymes to determine whether ischemia, injury, or infarct has occurred.
- Review serial electrolyte levels because disturbance in potassium or magnesium is a risk factor for dysrythmias.
- Review ABGs for hypoxemia and acidosis because these conditions increase the risk for dysrythmias, decreased contractility, and decrease tissue perfusion.
Patient Management - Provide supplemental oxygen to maintain or improve oxygenation. The patient may be intubated and mechanically ventilated.
- Minimize oxygen demand by maintaining bed rest.
- Be alert for dysrhythmias risk factor for anemia, hypovolemia, hypokalemia, hypomagnesemia and acidosis.
- Because most sudden cardiac death occurances are secondary to a lethal dysrhythmia, 24 hour Holter monitoring and possible electrophysiologic study (EPS) may be done to determine the effectiveness of pharmacologic regimen.
Related posts: - Cardiac Tamponade
- Hypovolemic Shock Patient Care and Monitoring
- Hypertensive Crisis
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