Medical Surgical Nursing – 41118 Lecture PDF

MEDICAL SURGICAL NURSING – 41118 Lecture PADAGAS, Francine Nicole J. Prelim / Midterm / Finals 5. ACUTE PANCREATITIS  15-20% are idiopathic (after work-up returns i...

MEDICAL SURGICAL NURSING – 41118 Lecture PADAGAS, Francine Nicole J. Prelim / Midterm / Finals 5. ACUTE PANCREATITIS  15-20% are idiopathic (after work-up returns inconclusive).  The exocrine pancreas stores many of the enzymes needed for digestion. Pathophysiology  Results from some trigger causing the body to "autodigest" the pancreas.  The enzymes (trypsin, phospholipase A, amylase and elastase) that the pancreas is storing are released within the pancreas (instead of being excreted to the duodenum) and the pancreas starts to break down.  Pancreas has a normal protective mechanism through an enzyme called trypsin inhibitor that prevents enzyme activation before they reach the duodenum.  Digestive enzymes:  Trypsin digests PROTEIN (N: 115-350 mg/ml).  Amylase digests STARCH (N: 19-86 U/L).  Lipase digests FATS (N: 7-59 U/L). Diagnosis: 2 out of 3 Criteria 1. Characteristic abdominal pain or epigastric pain that may radiate to the back. 2. Serum amylase or lipase values 2 to 4 times above the normal range.  In general, serum lipase is more sensitive than serum amylase as a marker of pancreatitis  Normal serum lipase: Clinical Manifestations  Normal serum amylase:  Acute pain: Severe, relentless, knifelike; midepigastrium 3. Characteristic findings on imaging (most often ultrasound or periumbilical imaging).  Abdominal guarding, rebound tenderness  Vomiting, nausea, hypoactive bowel sounds Scoring System: Disease Severity Bedside Index of Severity of Acute Pancreatitis (BISAP)  Fluid volume deficit  First 24 hours  Hypotension, mental status changes  Accurate and easy to use  Tachycardia, cool clammy skin, decreased urine The score is calculated on five variables: output 1. BUN > 25 mg/dL; 2. Impaired mental status;  Impaired gas exchange 3. Presence of two or more criteria of systemic  Decreased PaO2 (< 60 mmHg) and O2sat (< 90%) inflammatory response syndrome:  Body Temperature > 38 or < 36 degrees Celsius. Management  HR > 90 bpm. 1. FLUID RESUSCITATION - From fluid losses due to third  RR > 20 cpm or partial pressure of CO2 < 32 mmHg spacing losses, vomiting, and vascular permeability 2nd to  Leukocyte count > 12,000 or < 4,000/microliters or inflammatory mediators. over 10% immature forms or bands.  IV isotonic crystalloid fluids. 4. Age > 60 years old  Monitor for signs of retroperitoneal hemorrhage 5. Pleural effusion on imaging  Low hematocrit, Hgb  Grey Turner sign  Each variable provides one point.  Cullen sign  Scores of 3, 4, and 5 are associated with higher hospital  Monitor abdominal girth mortality.  Score of 5 associated with -22% rate of mortality EXERCISE Determine BISAP score of patient A with the following assessment parameters:  55 years old  BUN > 30 mg/dL  Stuporous  X-ray: Clear  O2 sat = 95%  Monitor for electrolyte imbalances (Ca, Na, Mg and  Temp: 38.5 C K+, glucose)  SCORE: 2 Etiology 2. PAIN MANAGEMENT  Chronic alcohol use  Caused by:  Gallstones/biliary tract disease  Peritoneal irritation from activated pancreatic  Less common exocrine enzymes. Drug induced:  Edema or distention of the pancreas.  Metronidazole  Interruption of the blood supply to the pancreas.  Tetracycline  Pain is a universal sign of AP, treatment is a priority  Azathioprine because it increases exocrine enzyme release  Estrogens  Opiates are generally discouraged. 1|P a g e   Assist the patient to a comfortable position (knee- ENDOCRINE DISORDERS chest position). 3. PREVENTING PANCREATIC STIMULATION.  Mild pancreatitis  Low-fat, low-residue oral feedings may be considered within the first 24 to 48 hours.  Moderate pancreatitis  EN with jejunal feedings is often preferred to prevent pancreatic stimulation and enzyme secretion.  PN is not necessary  unless EN feeding is not tolerated. 4. TREATING LOCAL COMPLICATIONS IN THE PANCREAS  Percutaneous or stent therapies to drain the fluids in and around the pancreas. Result from the action of TOO MUCH or TOO LITTLE hormone.  Surgical resection or debridement may be required if Diagnostic Tests the pancreas becomes infected.  Biliary ERCP or Laparoscopic Cholecystectomy (for  Fasting blood glucose level gallstone pancreatitis)  Glucose tolerance test  HbA1c Vascular Problems - Neuropathy leads to impaired sensation, numbness, tingling, weakness and muscle wasting - What are patients at risk for? NECROSIS 1. DIABETES MELLITUS  More commonly known just as "diabetes" is concerned with 2 hormones:  Insulin allows glucose into the cell, serum levels drop.  Glucagon converts glycogen into glucose, serum levels rise.  Glycogen storage form of glucose stored in the liver. 5. TREATING MULTISYSTEM FAILURE  Cardiopulmonary Complications  Most common multi system problem.  Pancreatic ischemia: Release of myocardial depressant factor → decreased myocardial output and contractility. o Administer O2 therapy. o Fluids, inotropes, and vasopressors.  Measure to prevent infection.  Manage coagulopathies.  Treat acute kidney injury (if it is a complicating factor.) TYPE 1  Actual INSULIN making cells are destroyed (beta cells) (autoimmune) TYPE 2  "Relative" deficit of insulin (decreased receptor sensitivity to insulin). THE 3 P’S 2|P a g e  a. Polyuria  Excess glucose spills into the urine and is excreted. This causes water to follow the higher osmotic pressure of the urine (increased water loss).  Electrolytes from the body also get excreted in large amounts. b. Polydipsia  Fluid loss through polyuria draws out water from the cells, leading to dehydration.  The body responds to dehydration by triggering the thirst mechanism.  This results in the "condition of much thirst"; lots and lots of water intake c. Polyphagia  Lack of nutrients (specifically glucose) entering the cells stimulates appetite in order to increase the amount of nutrients taken in.  This leads to the "condition of much eating;” the patient has intense appetite in the body's attempt to restore glucose to the cells. Complications  Diabetes has many potential short and long term complications.  Short term complications are hypoglycemic shock and diabetic ketoacidosis (DKA).  Long term complications result from increased glucose in the blood over a long period of time. A. Hypoglycemic Shock Development of DKA  Execss of insulin which causes deficit of glucose in the body  Can be caused when insulin is taken then skipping a meal, SEVERITY vomiting, error in dosage. The lack of glucose affects the a. Mild DKA nervous system b/c the neurons ca’t use fats or proteins as  Hyperglycemia (> 300 mg/dl) an energy source.  LOW BICARBONATE (15-18 mEq/L)  Brain does not need insulin to utilize glucose, but it does NEED  Acidosis (pH < 7.30) GLUCOSE in the circulation.  Ketonemia  Neurons can’t use fats or proteins as an energy source.  Ketonuria  Low blood glucose immediately affects CNS. The brain has no reserves of glucose. b. Moderate DKA  Usually occurs in patients with type 1 diabetes following  pH < 7.20 strenuous exercise or skipping a meal after taking insulin.  Serum bicarb (10-14 mEq/L)  Manifestations of hypoglycemia are directly due to lack of  Increasing drowsiness circulating glucose.  If hypoglycemia affects the CNS right away, what manifestations c. Severe DKA do you expect?  pH < 7.10  Poor concentration, slurred speech, staggering, appears  Bicarb < 10 mEq/L "intoxicated with alcohol.”  Decreased level of consciousness or coma  If hypoglycemia stimulates the sympathetic nervous system, what manifestations do you expect?  PREVENTION  Increased HR, anxiety, tremors, if left untreated loss of  "Sick day rules" consciousness, seizures and death will follow.  Never eliminate insulin doses when nausea and vomiting occurs. B. Diabetic Ketoacidosis (DKA)  Drinking fluids every hour.  Absence or markedly inadequate amount of insulin.  Blood glucose and urine ketones are assessed every 3-  The deficit results in disorders in the metabolism of 4 hours. carbohydrates, protein and fat.  If unable to retain oral fluids, hospitalization may be required.  Due to insufficient insulin. CLINICAL MANIFESTATIONS 3 MAIN CLINICAL FEATURES:  3Ps  Hyperglycemia  Marked fatigue  Ketonemia  Blurred vision, headache, weakness  Metabolic acidosis  Orthostatic hypotension with marked intravascular volume depletion. 3 MAIN CAUSES:  Ketosis and acidosis will cause Gl s/sx (usually causes them  Decreased or missed dose of insulin to seek medical attention)  Illness/infection  Anorexia  Undiagnosed and untreated diabetes  Nausea and vomiting  Abdominal pain  Acetone breath (fruity odor)  Kussmaul’s respiration: Body's attempt to decrease acidosis. MANAGEMENT  Correcting: 3|P a g e   Hyperglycemia  Dehydration  Long Acting  Electrolyte loss  Lantus  Acidosis a. REHYDRATION  Enhances excretion of excessive glucose by the kidneys.  May need as much as 6 to 10 L of IV fluid  Initially:  First 2 hours: 0.9% Sodium Chloride 0.5 L to 1 L per hour  for the patients with hypernatremia, hypertension and at risk for heart failure are given half strength NSS (0.45% NSS).  After several hours: Half strength NSS is given  Monitor:  Fluid volume status (VS)  Lung assessment  I&O b. RESTORING ELECTROLYTES.  Potassium: Major electrolyte of concern.  Normal value: 3.5-5.2 mmol/L  May be low, normal or high but more often than not, high due to disruption of cellular sodium-potassium pump (acidosis).  During rehydration, K+ may be decreased (due to increased urinary excretion, insulin administration moves potassium from extracellular fluid into the cells).  Potassium replacement is vital to avoid arrhythmias.  Withheld only if hyperkalemia is present.  Patient is not urinating. c. REVERSING ACIDOSIS. C. Hyperglycemic Hyperosmolar Syndrome (HHS)  Acidosis is reversed usually with insulin.  Metabolic disorder, most often of type 2 diabetes due to a relative  Insulin infused at a slow, continuous IV infusion rate (e.g. 5 insulin deficiency initiated by an illness raising the demand for units/hour). insulin.  IV fluid solutions with higher concentration of glucose are  Basic biochemical defect is lack of effective insulin (insulin given when blood glucose levels reach 250 to 300 mg/dL. resistance).  To avoid rapid drop in blood glucose during treatment.  Insulin is too low to prevent hyperglycemia (and subsequent osmotic diuresis) but it is high enough to prevent fat breakdown.  Insulin is infused continuously until SQ administration of  Main difference with DKA? insulin can be resumed.  Often occurs in older adults (50-70 y/o)  IV insulin is usually continued until serum bicarbonate increases at least 15-18 mEq/L. ASSESSMENT/DIAGNOSTIC FINDINGS  Hypotension What type of insulin is approved for IV infusion?  Profound dehydration (poor skin turgor, dry mucous  RAPID-ACTING INSULINS (HUMULIN R) membranes)  Tachycardia These three examples illustrate blood glucose management strategies  Variable neurologic signs (altered LOC, seizures, that may be used: hemiparesis, hallucinations - cerebral dehydration) 1. Patient A receives 3 units of continuous IV regular insulin per hour  Polyuria and has a blood glucose measurement of 110 mg/dL, but 1 hour  Polydipsia ago it was 190 mg/dL.  No GI symptoms  The insulin rate must be decreased to avoid sudden  Blood glucose > 600 mg/dL hypoglycemia. MANAGEMENT 2. Patient B receives 3 units of continuous IV regular insulin per hour  Fluid replacement and has a blood glucose measurement of 110 mg/dL, but 1 hour  0.9% NaCl ago it was 112 mg/dL.  Dextrose IV given once CBG is in the range of 250-300  In this situation, no change is made in the insulin mg/dl (like DKA). infusion rate  Correction of electrolyte imbalances.  Insulin administration. 3. Patient C receives 3 units of continuous IVregular insulin per hour  Still given at a slow continuous rate. and has a blood glucose measurement of 190 mg/dL, and 1 hour  Close monitoring of volume and electrolyte status is ago it was 197 mg/ dL. important to prevent fluid overload and cardiac  The insulin rate must be increased to move the arrhythmias (older adult) patient's blood sugar more rapidly toward the targeted glucose range (i.e., 140 to 180 mg/dL, although this range varies by individual hospital protocol. INSULIN TYPE, ONSET, & PEAKS  Short Acting  Lispro  Exubra  Regular Insulin  Intermediate Acting  NPH 4|P a g e