SAINT PAUL UNIVERSITY DUMAGUETE DUMAGUETE CITY COLLEGE OF NURSING SY 2011 2012

IN PARTIAL FULFILLMENT OF THE REEQUIREMENTS IN RELATED LEARNING EXPERIENCE PERPETUAL SUCCOUR HOSPITAL OPERATING ROOM

CENTRAL VENOUS ACCESS VIA TUNNELED ANTERIOR APPROACH TO THE INTER JUGULAR VEIN

Submitted to: Miss Azaleah Villasis, R. N. Clinical Instructor

Submitted by: Mr. Vaughn Spencer B. Visagas, SN - SPUD

I.

BIOGRAPHICAL DATA

Name: Mrs. G. R. R. Age: 74 years old Sex: female Address: Damintao, Bogo City, Cebu Reason for seeking health care: AV fistula dysfunction Operation Performed: Intrajugular Catheter Insertion Case Number: 96553 Surgeon: Dr. M. Perez Assistant Surgeon: Dr. L. E. Abelgas

II.

THEORETICAL BACKGROUND

Chronic Kidney Disease secondary to Hypertension, Nephrosclerosis Chronic kidney disease (CKD) is a worldwide public health problem. It is recognized as a common condition that is associated with an increased risk of cardiovascular disease and chronic renal failure (CRF). The Kidney Disease Outcomes Quality Initiative (K/DOQI) of the National Kidney Foundation (NKF) defines chronic kidney disease as either kidney damage or a decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for 3 or more months. Whatever the underlying etiology, the destruction of renal mass with irreversible sclerosis and loss of nephrons leads to a progressive decline in GFR. The different stages of chronic kidney disease form a continuum in time. In 2002, K/DOQI published its classification of the stages of chronic kidney disease, as follows: Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2) Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2) Stage 3: Moderate reduction in GFR (30-59 mL/min/1.73 m2) Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m2) Stage 5: Kidney failure (GFR < 15 mL/min/1.73 m2 or dialysis)

In stage 1 and stage 2 chronic kidney disease, GFR alone does not clinch the diagnosis. Other markers of kidney damage, including abnormalities in the composition of blood or urine or abnormalities on imaging studies, should also be present in establishing a diagnosis of stage 1 and stage 2 chronic kidney disease. The K/DOQI definition and classification of chronic kidney disease allow better communication among physicians and facilitate intervention at the different stages. a. Pathophysiology Approximately 1 million nephrons are present in each kidney, each contributing to the total GFR. In the face of renal injury (regardless of the etiology), the kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, by hyperfiltration and compensatory hypertrophy of the remaining healthy nephrons. This nephron adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances such as urea and creatinine start to show significant increases only after total GFR has decreased to 50%, when the renal reserve has been exhausted. The plasma creatinine value will approximately double with a 50% reduction in GFR. A rise in plasma creatinine from a baseline value of 0.6 mg/dL to 1.2 mg/dL in a patient, although still within the reference range, actually represents a loss of 50% of functioning nephron mass. The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive renal dysfunction. This is believed to occur because of increased glomerular capillary pressure, which damages the capillaries and leads initially to secondary focal and segmental glomerulosclerosis and eventually to global glomerulosclerosis. This hypothesis has been based on studies of fivesixths nephrectomized rats, which develop lesions identical to those observed in humans with chronic kidney disease. Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following: Systemic hypertension Acute insults from nephrotoxins or decreased perfusion Proteinuria Increased renal ammoniagenesis with interstitial injury

Hyperlipidemia Hyperphosphatemia with calcium phosphate deposition Decreased levels of nitrous oxide Smoking Uncontrolled diabetes

b. Common Etiology Causes of chronic kidney disease include the following: Diabetic kidney disease Hypertension Vascular disease Glomerular disease (primary or secondary) Tubulointerstitial disease Urinary tract obstruction

Vascular diseases that can cause chronic kidney disease include the following: Renal artery stenosis Cytoplasmic pattern antineutrophil cytoplasmic antibody (C-ANCA) positive and perinuclear pattern antineutrophil cytoplasmic antibody (P-ANCA)positive vasculitides Antineutrophil cytoplasmic antibody (ANCA)negative vasculitides Atheroemboli Hypertensive nephrosclerosis Renal vein thrombosis Unrecovered acute kidney injury Primary glomerular diseases include the following: Membranous nephropathy Immunoglobulin A (IgA) nephropathy Focal and segmental glomerulosclerosis (FSGS) Minimal change disease Membranoproliferative glomerulonephritis

Rapidly progressive (crescentic) glomerulonephritis Secondary causes of glomerular disease include the following: Diabetes mellitus Systemic lupus erythematosus Rheumatoid arthritis Mixed connective tissue disease Scleroderma Goodpasture syndrome Wegener granulomatosis Mixed cryoglobulinemia

Postinfectious glomerulonephritis Endocarditis Hepatitis B and C Syphilis Human immunodeficiency virus (HIV) Parasitic infection Heroin use Gold Penicillamine

Causes of tubulointerstitial disease include the following: Drugs (eg, sulfa, allopurinol) Infection (viral, bacterial, parasitic) Sjgren syndrome Chronic hypokalemia Chronic hypercalcemia Sarcoidosis Multiple myeloma cast nephropathy Heavy metals Radiation nephritis Polycystic kidneys Cystinosis

Urinary tract obstruction may result from any of the following: Urolithiasis Benign prostatic hypertrophy Tumors Retroperitoneal fibrosis Urethral stricture Neurogenic bladder

III. SURGICAL MANAGEMENT Central Venous Access via Tunneled Anterior Approach to the Internal Jugular Vein Central venous access is essential in providing quality medical care to many patients for whom intensive therapy is required. In many situations, a semipermanent tunneled central line is preferred (see Indications). An anterior approach to the internal jugular vein is the best option in this situation because it offers the easiest route with a low risk of complications. In this procedure, a tunneled catheter is surgically inserted into a vein in the neck or chest and passed under the skin. Only the end of the catheter is brought through the skin; medicines and intravenous fluid can be administered through this catheter; other tasks, such as blood sampling, can also be performed. The fact that the catheter is passed under the skin helps secure the catheter, reduces the rate of infection, and permits free movement of the catheter port. The placement of a tunneled catheter should be carried out by practitioners with specific experience in the procedure.

a. Indications Complex or critically ill patients who need continuous hemodynamic monitoring Patients who require secure venous access for the infusion of agents that are very irritating or that have a very narrow therapeutic index, and which, therefore, require a very precise rate of delivery into the circulation (eg, cytotoxic drugs, inotropic agents) Patients who require long-term venous access for parenteral nutrition, chemotherapy, or long-term prophylactic antibiotics Patients in whom very frequent blood sampling or access to the circulation for other reasons is needed Patients in whom venous access cannot be secured by any other route.

b. Contraindications This procedure has no absolute contraindications include the following: contraindications. Relative

Severe coagulopathy Physical status unfit for anesthesia Unavailability of a suitable access site Thrombosed veins Overlying skin infection In patients who need long-term venous access (eg, patients with small bowel transplant), imaging of the neck veins may be necessary before the procedure. Doppler ultrasound (US) and/or magnetic resonance (MR) venography can establish venous patency and anatomy, thus improving planning and anticipation of potential problems with access.[1] Particularly in patients with multiple medical problems, a complete blood count, clotting profile, and relevant renal and liver function tests should be included in the preoperative workup. Depending on the platelet count, platelet transfusion may be needed.

c. Anesthesia A local anesthetic agent is used before tunneling the catheter. d. Equipment Central venous catheter

e. Positioning Trendelenburg position with the head turned to the opposite side of the central venous line (CVL) insertion is optimal, as the internal jugular vein (IJV) distends in this position, providing a maximal cross-sectional area for access. The ipsilateral arm should be extended minimally at the axilla.

f. Preventive Measures To prevent line sepsis, use a full aseptic technique, including the following:

Chlorhexidine preparation Full draping Minimal handling of the line (no-touch technique) Care when using ultrasonography for guidance

Before use, flush the line and accessory devices (dilators, wires, peel-off sheath) with saline. Ultrasound-guided insertion requires familiarity with the probe, image acquisition, orientation, and interpretation. ECG monitoring of the patient is necessary to alert the operator to the occurrence of dysrhythmias. Heparin flush should be used at the end of procedure and subsequently to preserve patency when the line is in infrequent use. Prompt recognition and treatment of line sepsis is important. Especially in neonates and infants, a chronic line infection may have a subtle presentation, with increasing bilirubin, falling platelet count, and low-grade pyrexia. Suspicion of line sepsis requires prompt and repeated testing for microbiology, including testing for fungi. Line sepsis requires aggressive treatment with intravenous antibiotics as per institutional protocol. Early removal is advocated to avoid loss of veins.

Avoid line placement in the following sites: Damaged skin sites (eg, infection, burn, radiotherapy) Mastectomy/axillary node dissection, other surgery sites Pacemaker wires Breast prosthesis

g. Complications Intraoperative Arterial puncture/catheterization Hematoma formation Air embolism Hemothorax Pneumothorax Chylothorax Misplaced line Multiple attempts leading to damage to adjacent structures (esophagus, trachea, recurrent laryngeal nerve, vagus nerve)

Dysrhythmias Cardiac perforation/tamponade Postoperative Bleeding Pain Thrombosis Sepsis Pinch-off syndrome (compression of the line between the clavicle and first rib) Catheter block Catheter fracture