Goals: To provide quality care to patient under surgery.

Objectives: 1. 2. 3. 4. 5. To lessen the anxiety level of the patient. To lessen the pain of the patient. To know the benefits of these procedure to her health. Clients educate about the reason behind the disease.

Introduction Cholecystitis is defined as inflammation of the gallbladder and is traditionally divided into acute and chronic subtypes. These subtypes are considered to be 2 separate disease states; however, evidence suggests that the 2 conditions are closely related, especially in the pediatric population. Most gallbladders that are removed for acute cholecystitis show evidence of chronic inflammation, supporting the concept that acute cholecystitis may actually be an exacerbation of chronic distension and tissue damage. Cholecystitis may also be considered calculous or acalculous, but the inflammatory process remains the same. Cholecystitis, which has long been considered an adult disease, is quickly gaining recognition in pediatric practice because of the significant documented increase in nonhemolytic cases over the last 20 years. Gallbladder disease is common throughout the adult population, affecting as many as 25 million Americans and resulting in 500,000700,000 cholecystectomies per year (see Epidemiology). The image below illustrates the technique for laparoscopic cholecystectomy. Chronic cholecystitis is most often related to gallstone disease but has been documented without gallstones. Its course may be insidious or involve several acute episodes of obstruction. The initiating factor is thought to be the supersaturation of bile, often with cholesterol crystals and/or calcium bilirubinate, which contributes to stone formation and inflammation. These processes lead to chronic obstruction, decreased contractile function, and biliary stasis, which contribute to further inflammation of the gallbladder wall. Biliary stasis also permits the increased growth of bacteria, usually Escherichia coli and enterococci, which may irritate the mucosa and increase inflammatory response. Chronic acalculous cholecystitis is less understood, but it may result from a functional deficiency of the gallbladder, which leads to spasm and an inability to appropriately empty the gallbladder contents, causing chronic bile stasis. Acute calculous cholecystitis results from a more sudden obstruction of the cystic duct by gallstones, which causes distension of the sac, edema, and bile stasis with bacterial overgrowth. These events lead to inflammation and a local release of lysolecithins, which further exacerbates the inflammatory process. In addition, edema of the wall and duct reinforces obstruction and may cause ischemia of the local tissue, with the release of still more inflammatory mediators. Local lymph node hypertrophy and duct torsion or congenital anomalies may further complicate the obstructive process. As obstruction and inflammatory tissue damage progress, bacteria may proliferate. Bile cultures are positive in 75% of cases, usually with

E coli, enterococci, or Klebsiella species. Bacterial infection most likely follows tissue damage, but after colonization, the severity of the disease can dramatically worsen. This cascade of events quickly leads to pain and, possibly, a toxic appearance. Acute acalculous cholecystitis develops in a similar manner but from different etiologic factors than acute calculous cholecystitis does. Acute acalculous cholecystitis is most often associated with systemic illness, whether chronic or critical and acute. Increased mucus production, dehydration, and increased pigment load all increase cholesterol saturation and biliary stasis, whereas hyperalimentation, assisted ventilation, intravenous narcotics, ileus, and prolonged fasting contribute to cholestatic hypofunction. These conditions allow the formation of biliary sludge and may lead to obstruction. The resulting inflammation and edema lead to compromised blood flow and bacterial infection, as in acute calculous cholecystitis; however, the compromised blood flow appears more central in acute acalculous cholecystitis because acute acalculous cholecystitis can occur in vasculitides (eg, Kawasaki disease, periarteritis nodosa), presumably because of direct vascular compromise. Cholelithiasis in infancy is most often related to acute and chronic illness and hyperalimentation. More specifically, risk factors include abdominal surgery, sepsis, bronchopulmonary dysplasia, hemolytic disease, malabsorption, necrotizing enterocolitis, and hepatobiliary disease. Other factors implicated include CF, polycythemia, phototherapy, and distal ileal resection. The immature hepatobiliary system of infants may predispose them to stone formation. Decreased hepatobiliary flow and immature bilirubin conjugation contribute to stasis and sludge formation. Interestingly, as much as one half of infantile gallstones, especially those associated with hyperalimentation, may resolve spontaneously. In a review of 693 cases of pediatric cholelithiasis by Friesen et al, infants with the disease tended to be ill and receiving hyperalimentation, and had prematurity, congenital anomalies, and necrotizing enterocolitis as compounding risk factors. Risk factors for cholelithiasis in children include hepatobiliary disease, abdominal surgery, artificial heart valves, and malabsorption. Gallstones usually contain a mixture of calcium bilirubinate and cholesterol. Hemolysis and prolonged hyperalimentation are significant influences in this age group. (In the Friesen study, hemolysis was the most common underlying condition for cholelithiasis in children aged 1-5 years). In adolescents, risk factors for cholelithiasis include pregnancy, hemolytic disease, obesity, abdominal surgery, hepatobiliary disease, hyperalimentation, malabsorption, dehydration, and the use of birth control pills.

Demographic data: Name: Arlando Judy Ann Age:15 yrs old Birthday:9-8-95 Civil Status: Single Surgeon: Dr. Villacorta Anesthesiologist: Dr. Agulla Indication of the procedure: 6 days of PTA colic RUQ abdominal pain sudden radiaty to back gr 10/10 5days PTA consult to UTZ gallstone, Tx buscopan, patient was referred to AP Hence admission Due to her chief complaint of pain in the abdomen.

Operations perform: Open cholecystectomy

Final Diagnosis: Acute calculous cholecystitis

NCP (pre) Assessment S: No verbal cues O: Bp: 120/80 mmHg PR: 62 bpm RR: 18 cpm T: 36.5 Afebrile Warm to touch Pale looking Nsg Diagnosis Fear r/t surgical procedure Planning Within 8 hours of nursing intervention the patient will lessen the anxiety prior to the procedure. Intervention Received patient for OR per stretcher accompanied by NOD - With ongoing IVF infusing well - Pre assessment done - Transferred to OR2 safety then hooked to oxygen & cardiac monitoring - Place the client in side lying position - Lumbar prepping done aseptically induction - Induction of anesthesia care of Cr. Agulla aseptically - Placed patient Evaluation Within 8 hours of nursing intervention the patient lessened anxiety level or fear.

back into supine position Foley catheter done aseptically

(Post) Assessment O: Bp: 130/70 PR: 60 RR: 20 Nsg Diagnosis Risk for infection r/t inadequate primary defense of broken of the skin Planning Within 8 hours of nursing intervention the patient will decrease the risk for infection Intervention Abdominal prepping done aseptically Sterile drape done aseptically initial counting of skin done by layered Specimen out Observed the inside part of the gall bladder Stone out in the billiary Clamping done Suturing started Evaluation Within 8 hours of nursing intervention the patient decrease the risk for infection

Counting of APRs, sponges, instruments done complete AP informed Suturing of the muscle 2nd & final counting of APRs , sponges, instrument done completely connect Continue suturing up to the skin Procedure ended Endorsed

(Post)

Assessment O: BP:120/90 PR: 75 RR: 25 -facial grimace -pain scale of 10

Diagnosis Within 8 hours of nursing intervention the patient will decrease pain from 10 to 9

Planning Acute pain r/t surgical incision

Intervention Flat on bed Oxygen until full awake - Vital sign every 15 minutes - IVF infusing well - NPO Encouraged the patient to do deep breathing exercise

Evaluation Within 8 hours of nursing intervention the patient decreased pain from 10 to 8