Week-1-fluids-and-access_100553_284_11749_v1-1cvvlu2.pdf

Fluids and Access Joseph Donroe, M.D., M.P.H. Mark A. Perazella, M.D. Shyoko Honiden, M.D.

Goals: 1. Identify the main IV fluids available for resuscitation and maintenance purposes and the advantages to each 2. Know the different types of access and which ones are appropriate for rapid resuscitation 3. Identify the indications for administering sodium bicarbonate 4. Know the principles of fluid management in hypernatremia, hyponatremia due to SIADH and liver failure. Case One: A 36-year-old (70kg) male presents to the ED febrile with HR 120bpm, RR 35 bpm and blood pressure of 80/50. Initial work -up reveals a WBC of 14,000 and multi-lobar consolidations on chest x-ray. Early goal directed therapy for severe sepsis due to pneumonia is initiated.

1. You ask the nurse to obtain access. How many, and what sized, IVs would you like placed? Given the option of delivering IV fluid through a peripheral IV or a standard central line, which will you choose? Peripheral IVs vary in caliber from very large (12g) to very small (27g). For resuscitation purposes, at least two “large bore” IVs should be placed, meaning IV catheters size 12-16 gauge. Note that smaller “gauge” catheters have larger calibers. Central lines are measured in “french” units rather than “gauge” and larger “french” catheters have larger calibers. The speed at which fluids can be delivered is governed by the Hagen-Poiseuille equation which states that rate of flow through a tube is directly related to the radius of the tube to the fourth power and inversely related to the length of the tube. Thus, maximal infusion speed is obtained by delivering fluids via a fatter, shorter catheter. Standard large bore IV (usually 35cm long) will infuse faster than a standard triple lumen central venous catheter (typically 7 French and 20 cm long). An introducer catheter (commonly referred to by the manufacturer name: Cordis) is occasionally used in traumas or massive GI bleeds and gives the highest infusion rates because of its large caliber (usually 8.5 to 9 Fr) and relatively short length (usually 10 to 13 cm). For most early goal directed therapy scenarios introducer catheters are not necessary.

2. After the two 16g peripheral IVs are placed, which intravenous fluid (IVF) will you order for the initial resuscitation and how much will you give? Does it matter if we use crystalloid or colloid? There are three elements to consider: • What tonicity of fluid to infuse? • What composition of fluids to infuse? • What infusion rate and volume to order? The answers depend on the clinical scenario. • What tonicity of fluid to infuse? The goal of fluid resuscitation is to augment cardiac output by increasing preload, thus it is desirable to give fluids that will be maintained in the intravascular space. Tonicity refers to the osmolarity of the infusate relative to plasma and governs how the infusate will distribute within the body’s different fluid compartments. Isotonic solutions are maintained in the extracellular fluid compartment (composed of the intravascular + interstitial spaces) while hypotonic fluids distribute across the entire body water (extracellular space and the much larger intracellular space). Since most of the volume of hypotonic solutions redistributes out of the intravascular space and into the intracellular compartment, hypotonic solutions should be avoided is resuscitation. Figure 1 illustrates the different fluid compartments. •

What composition of fluid to infuse? The broad categories of fluids are crystalloids and colloids. The relative compositions of several common IVF are included in Table 1.

Table 1: Composition of crystalloids and colloids Plasma

Na (meq/L) 140

K (meq/L) 4

0.9% NS LR

154 130

4

PRBC 5% Albumin 25% Albumin 6% Hetastarch

140

4

IVF

Hextend

130-160 130-160 154 143

0.45% NS 77 0.225%NS 34 D5W * Marino PL., 2007

3

Cl Ca Other (meq/L) (meq/L) 103 5 25-bica Isotonic Crystalloid Solutions 154 109 3 28-lact Isotonic Colloid Solutions 103 5 RBCs 5g alb/ 100ml 25g alb/100ml Hydroxyethyl 154 starch 28-lactate 0.9- Mg 125 5 6% hetastarch Hypotonic Solutions 77 34

mOsm

pH

Cost/L*

290

7.4

308 273

5.7 6.4

1.46 1.48

~290

“physiologic”

122.50

~290

“physiologic”

612.60

309

5.5

55.26

307

5.9

290

154 68 252

The isotonic crystalloid options are largely equivalent, although a disadvantage of 0.9% normal saline (NS) is the resulting non-anion gap hyperchloremic metabolic acidosis when used for large volume resuscitation. Lactated ringers (LR) solution should be used cautiously in renal or liver failure. Non-blood colloids are albumin or starch based solutions diluted in isotonic saline. They differ from isotonic crystalloid solutions in that they add intravascular oncotic pressure leading to increased retention of fluid in the intravascular compartment. For each liter of 5% albumin infused approximately 700ml remains in the intravascular compartment (compared to 300cc/L NS). It is typically administered in 250-500ml aliquots. Six percent hetastarch solutions have plasma expansion properties similar to those of 5% albumin solutions. While there is greater expansion of the intravascular space per unit volume of colloid given compared to isotonic crystalloid, after much study and debate crystalloids remain the IVF of choice for most resuscitation scenarios. Studies have failed to identify any mortality benefit to colloid resuscitation compared to crystalloid (a Cochrane Review from 2004 actually suggests an increased mortality with albumin resuscitation in critically ill patients) and the cost of colloids is much greater (see table). A study by Brunkhorst in 2008 also noted that in patients with severe sepsis or septic shock there was a significantly increased risk of acute renal failure and extended need for renal replacement therapy, as well as a non-significant trend towards increased mortality in those receiving hetastarch compared to lactated ringers solution (Brunkhorst FM, Engel C, Bloos F, et al., 2008). •

What infusion rate and volume to order? The initial IVFs should be administered in boluses to a hemo-dynamically unstable patient. The 2008 “Surviving Sepsis Campaign” suggests giving fluid challenges of 1000ml of isotonic crystalloid or 300-500ml of colloid delivered over 30minutes with frequent evaluation of hemodynamic response (Dellinger RP, Levy MM, Carletet JM, et al., 2008). Greater volume and infusion rates may be needed depending on the severity of illness; critically ill patients can need as much as 10L of crystalloid in the initial resuscitation period. Adults with depressed ejection fractions or with renal failure may need a more conservative strategy with crystalloid fluids delivered in 500ml increments. As there are risks to aggressive fluid resuscitation, such as pulmonary edema and abdominal compartment syndrome, the impact of IVF therapy needs to be constantly reassessed using hemodynamic parameters (blood pressure, heart rate, urine output and central venous pressure (CVP)). Early goal directed therapy (EGDT) targets a CVP of 8mmHg (12 mmHg if mechanically ventilated). Since the CVP depends on a patient’s cardiac ventricular compliance, it is best interpreted as a

reflection of relative rather than absolute intravascular volume and should be interpreted in the context of other hemodynamic variables. In summary for this patient, boluses of isotonic solution (either normal saline or lactated ringers) should be administered in 1000ml increments at a minimum of 30 minutes per liter. Adjust the rate of delivery and volume of infusion depending on the hemodynamic response to the initial fluid resuscitation effort. Bonus: Why does peripheral edema commonly occur after large volume fluid resuscitation? In part, this is due to the sepsis capillary leak phenomenon, but another contributing factor is how isotonic fluids distribute within the body. They eventually distribute approximately evenly within the extracellular fluid compartment, composed of the intravascular (25%) and interstitial (75%) spaces. Thus, for each liter of isotonic crystalloid solution infused approximately 750-800cc will go to the interstitial space leading to edema.

Case One Continued: He is eventually intubated as his mental status wanes. Six liters of normal saline are given in the initial resuscitation effort and norepinephrine has been initiated and is being titrated up to keep his MAP >65. Relevant labs include: ABG 7.0/20/75/5 on 60% FiO2, an anion gap of 19 and lactic acid of 8. He remains tachycardic, with minimal urine output and his CVP is 6.

3. When is sodium bicarbonate indicated and how should it be administered? A recent study documenting extensive differences in practice between nephrologists and intensivists with respect to bicarbonate therapy to treat acidemia highlighted the considerable uncertainty surrounding this topic (Kraut JA, Kurtz I., 2006). For any patient with a metabolic acidosis driven by organic acid accumulation, the following should be considered in order to determine if bicarbonate therapy is warranted: •

•

•

What are the deleterious effects of severe acidemia: Severe acidemia can lead to impaired cardiac contractility, decreased cardiac output, and a fall in blood pressure. It limits the effectiveness of vasopressors and can potentiate cardiac arrhythmias. Low pH also influences the metabolism of many medications (acetylsalicylic acid, methotrexate, phenobarbital, phenytoin) and can increase their toxicity. When is acidemia severe enough to merit bicarbonate therapy: Most experts agree that bicarbonate therapy is indicated with pH<7.1, but this is not a hard and fast rule and should be individualized to the patient and underlying process. If the underlying process maintaining the acidosis can be reversed quickly (i.e. insulin administration to stop ketogenesis in DKA), sodium bicarbonate infusion is less useful. How much bicarbonate should be given: The amount of sodium bicarbonate to give depends on the calculated bicarbonate deficit, calculated as follows:

bicarbonate deficit (meq/l) = (desired [bicarb] – measured [bicarb]) x 0.7(body wt in Kg). The desired [bicarb] is the concentration of bicarbonate needed to increase the pH to 7.2 given a static PaCO2: [bicarb]= 0.4 [PaCO2] This will inevitably underestimate the desired bicarbonate because it does not account for the rise in PaCO2 that will accompany the rise in pH. •

What are the deleterious effects of bicarbonate therapy: The lack of mortality benefit has been consistent across studies and several studies have noted an association between bicarbonate therapy and increased mortality. A “paradoxical” intracellular and CNS acidosis can occur as bicarbonate is metabolized to CO2 which then diffuses intracellularly and across the blood brain barrier. There is also a fall in ionized calcium with alkali administration and a rebound alkalemia can result as organic acid metabolism replenishes the body’s own bicarbonate stores. Increasing arterial pH may also shift the oxy-hemoglobin dissociation curve to the left resulting in decrease O2 delivery at the tissues. Finally, hypernatremia and volume overload can result.

It is reasonable to consider sodium bicarbonate in this patient given the severity of his acidemia and poor response to norepinephrine. Desired [bicarbonate] to achieve a pH of 7.2: 0.4 x 20 = 8meq/L Bicarbonate Deficit: (8-5) x 0.7(70) = 147mEq ~150 mEq The goal would therefore be to deliver approximately 150mEq of bicarbonate: This can be accomplished by mixing three ampoules of sodium bicarbonate with 850cc of D5W and infused over 1-2 hours (1 amp or 50 mls contains 50mEq of sodium bicarbonate). An ABG should be repeated and subsequent dosing of bicarbonate can be done based upon the results. Case One Continued: After his first liter of sodium bicarbonate solution, his repeat ABG is 7.2/20/8 and his MAP is 70 on a moderate infusion of norepinephrine. No further sodium bicarbonate is given. Over the next 24 hours his condition stabilizes, he comes off of norepinephrine and is extubated. While being monitored in the ICU, he complains of abdominal pain. Abdominal x-rays are suggestive of an ileus. Your surgical consultant recommends bowel rest and serial exams.

4. After making him NPO, how will you determine his maintenance fluid requirements? Maintenance fluids should consider one’s water, electrolyte, and carbohydrate needs. Water needs can be estimated from the following equation, which is based on lean body weight, basal metabolic rate (BMR, measured as kCal) and the assumption that 1ml of water= 1kCal of BMR: 100kCal/kg/day for the first 10kg + 50kCal/kg/day for the next 10kg + 20kCal/kg/day for each subsequent kg, generally capped at 80kg. For this patient, his estimated maintenance water requirement is 1000 + 500 + 1000 = 2500 ml/day, or about 105ml/hr. Since water is required to produce urine and to dissipate the heat generated by metabolism, requirements are decreased for an anuric patient and increased with higher metabolic demand (i.e., fevers). Sodium needs can be calculated as 2-4meq/100Kcal/day; potassium as 12meq/100Kcal/day. Our patient needs 50-100meq/day of Na and 25-50meq/day of K. Since he will receive 2.5liters of fluid over 24 hours, this can easily be achieved with 0.45%NS (75meq Na per liter) with 20meq K added to each liter bag. Dextrose in the form of D5 (5% dextrose solution, or 5g dextrose/ 100ml solution) should be part of the maintenance fluids in a patient who is not getting any other carbohydrate source, though should be used cautiously in diabetic patients.

Case Two: A 60 kg, 42 year old female with known SIADH presents to the ED after a seizure and is found to have a serum sodium of 112meq/L and urine osmolarity of 600 mOsm/L. Family members note that last night she began acting confused. You are called down to the emergency department to assist in her management and arrive just as the ED team is preparing to infuse a liter of normal saline. During your evaluation she begins to seize again.

5. What recommendations will you make? Several principles of sodium correction pertain to this case. First, this initial rate of sodium correction should be faster for symptomatic hyponatremia as the risk of further seizures and coma outweighs the risk of osmotic demyelination. Second, the goal should be to raise the serum sodium by 8-10meq/L over 24h and approximately 18meq/L over 48 hours. Third, calculated rates of sodium correction should serve as rough guides, and the sodium levels need to be checked frequently and therapy adjusted to assure that the desired rate of correction is being met. Finally, isotonic saline has no role in the correcting hyponatremia due to SIADH, because the osmolarity of the infusate IVF must be greater than the urine osmolarity in order for the serum sodium to have a sustained increase (see explanation at end of case). A suggested approach to this patient would be as follows: Initially, the patient is severely symptomatic (seizing) presumably from hyponatremic encephalopathy (CEREBRAL EDEMA) and her sodium imbalance needs to be corrected quickly. Aim to increase her serum sodium by 4-6meq/l in the first 1-2 hours. This can be done by infusing 3% saline solution in 100cc boluses every ten minutes until her condition improves or up to three times (Moritz ML, Ayus JC., 2010). Case Two Continued: After the second bolus of 3%saline, she stops seizing but remains lethargic and confused. Repeat serum sodium after two hours of managing this patient is 116meq/L. At this point she remains moderately symptomatic (lethargy, confusion)

6. What will you do with her fluids now? The rate of sodium correction can be slowed. A reasonable target would be to increase the serum sodium to 120meq/L over the next 4-6 hours. We can calculate the initial expected change in serum sodium for each liter of infusate as follows: [(Infusate Na + Infusate K) – actual Na]/total body water (TBW) + 1 = change in serum Na/liter infusate

In this case: (513-116) / (60 x 0.5) + 1 = 12.8 meq/L In order to raise the serum sodium to 120 (a change of 4meq) we should infuse 313 ml of 3% normal saline solution. Due to the severity of her illness we can infuse this over six hours, or at a rate of approximately 50cc/h, checking serum sodium every two hours. Case Two Continued: Her serum sodium is checked every two hours and the rate of correction is approximately 1meq/h. After the 6 hour infusion her Na is 120 and her mental status is improved.

7. What will you recommend now with her IVF? At this point the serum sodium should be maintained at approximately this level such that the total change in sodium over 24h remains less than 10meq/L. After 24 hours, we can aim to slowly and steadily increase her sodium. This can be done in several ways: • Free water restriction: if her urine osmolarity remains 600mOsm/L, restricting her to 1L of free water daily should produce a slow and steady rise in her serum sodium. • If water restriction is not effective, she is likely either not compliant with the water restriction or her solute intake is insufficient. In either case, sodium chloride tablets can be added. A 1g salt tab has approximately 17meq of Na, or 34mOsm. Three to four grams of salt tabs TID should increase her water excretion and raise her serum sodium. • Add a loop diuretic. This will effectively lower her urine osmolarity and increase the kidneys capacity to excrete free water. • Add a vasopressin receptor antagonist (rarely required and very expensive!). Example: If a patient whose Uosm is 600mOsm/L receives 1L of normal saline (308mOsm/L), she will ultimately excrete the 308meq of solute in 500cc of free water (giving her a urine osmolarity of 600mOsm/L) and retain the extra 500ml of free water. To calculate change in serum sodium per liter of retained free water: Total body sodium = serum sodium x TBW: (112meq/L) (60kg x 0.5) = 3360meq New serum sodium= total body sodium/new TBW: (3360meq)/(60x0.5) +0.5L = 110meq/L

Case Three: A 45-year-old 70kg male with a history of profound cognitive impairment and PEG tube is admitted to the ICU obtunded and with a serum sodium of 168 mEq/L. He is hemo-dynamically stable.

8. How would you bring his sodium down safely? This patient has a deficit of free water relative to sodium, thus the treatment is free water replacement. Since brain edema can result from overly rapid correction, serum sodium should safely be lowered by at most 12meq/L/d. In general, the more acutely a patient becomes hypernatremic (or hyponatremic) the faster they can be safely corrected. The following outlines one approach to correction: • •

•

Calculate the free water deficit: [(current Na/desired Na)-1] x TBW Here, the free water deficit is 6.6L. Determine the rate of correction: Correcting to 145 at a rate of 0.5meq/L/h would take approximately 46 hours (168-145= 23meq/L; (23meq/L)/(0.5meq/L/h) = 46h). Replacement of the free water deficit will only correct the serum sodium if it is given above the maintenance needs of the patient. Assuming maintenance requirement of 2 L/day, this patient would require 10.6 liters over two days, or a rate of 220ml/hr. This is too high for most patients. Correcting over four days would give us a more reasonable rate of 150ml/h. Free water can also be replaced enterally via his PEG tube as well with appropriate boluses of free water added to his enteral feeds (i.e. 400cc free water Q 6hrs gives him an extra 1600cc of free water daily). Determine the type of fluid to administer: While any hypotonic solution delivered at an appropriate rate should lead to correction of the hypernatremia, D5W will require the lowest overall volume because it delivers the most free water/L infusate.

Case Four: A 40-year-old female with ESLD decompensated by ascites is admitted with sepsis. Paracentesis reveals 600 nucleated cells with neutrophilic predominance. Should this patient receive albumin?

9. What are the indications for albumin in ESLD? There are three evidence based indications for albumin in ESLD. These are as follows: • Prevention of acute kidney injury (AKI) in spontaneous bacterial peritonitis (which we assume this patient has): She should receive 1.5g/kg of albumin (given as 25% albumin) on day 1 followed by 1.0g/kg of albumin 72 hours later. This has been shown to decrease the incidence of AKI, which occurs in 30-40% of those with SBP, and reduce mortality (Sort P, Navasa M, Arroyo V, et al, 1999). • Prevention of post paracentesis circulatory dysfunction: This is typically given concurrently with large volume paracentesis where >5L of ascites is taken off. Eight grams of

•

albumin/L ascitic fluid removed should be given (this can be given as a 25% albumin solution). Studies have shown that this decreases the likelihood of post paracentesis circulatory dysfunction; however there has not been a consistent survival benefit (Wong F., 2007). Management of hepatorenal syndrome (HRS): In cases of HRS, volume expansion with an albumin infusion (typically given as 25g of albumin BID) in addition to vasoconstrictors, is given for a limited period of time. In cases of AKI in patients with ESLD, cessation of diuretics plus volume expansion with albumin for 48 hours may be useful in distinguishing HRS from classic pre-renal azotemia, as patients with HRS will not improve whereas those with pre-renal azotemia will have improvement in kidney function.

Primary References: 1. Sansivero GE. Features and selection of vascular access devices. Semin Oncol Nurs. 2010 May;26(2):88-101. http://dx.oi.org/ 10.1016/j.soncn.2010.02.006 2. Stevens W. Fluid balance and resuscitation: Critical aspects of ICU care. Nurs Crit Care. March 2008; 3(2). http://dx.doi.org/10.1097/01.CCN.0000313327.58868.c1

Additional References: 1. Reddick AD, Ronald J, Morrison WG. Intravenous fluid resuscitation: was Poiseuille right? Emerg Med J 2011;28:201-202. 2. Dellinger RP, Levy MM, Carletet JM, et al. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36 (1). 3. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med 1999;341:403–9. 4. Gines P, Arroyo V. Is there still a need for albumin infusions to treat patients with liver disease? Gut 2000;46: 588–590. 5. Wong F. Drug insight: the role of albumin in the management of chronic liver disease. Nat Clin Pract Gastroenterol Hepatol 2007 Jan;4(1):43-51. 6. Alderson P, Bunn F, Lefebvre C, et al. Human albumin solution for resuscitation and volume expansion in critically ill patients. Cochrane Database Syst Rev. 2004 Oct 18;(4):CD001208. 7. Moritz ML, Ayus JC. 100 cc 3% sodium chloride bolus: a novel treatment for hyponatremic encephalopathy. Metab Brain Dis (2010) 25:91–96. 8. Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000 May 25;342(21):1581-9. 9. Kraut JA, Kurtz I. Use of base in the treatment of severe acidemic states. Am J Kidney Dis 2001 Oct;38(4):703-27. 10. Kraut JA, Kurtz I. Use of base in the treatment of acute severe organic acidosis by nephrologists and critical care physicians: results of an online survey. Clin Exp Nephrol 2006 Jun;10(2):111-7. 11. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th edition. USA. The McGraw-Hill Companies, Inc. 1994. 12. Marino PL. The ICU Book, 3rd edition. Philadelphia, PA. Lippincott William and Wilkins. 2007. 13. Brunkhorst FM, Engel C, Bloos F, et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med 2008 Jan 10;358(2):125-39.

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Seminars in Oncology Nursing, Vol 26, No 2 (May), 2010: pp 88-101

FEATURES AND SELECTION OF VASCULAR ACCESS DEVICES GAIL EGAN SANSIVERO OBJECTIVE: To review venous anatomy and physiology, discuss assessment parameters before vascular access device (VAD) placement, and review VAD options.

DATA SOURCES: Journal articles, personal experience. CONCLUSION: A number of VAD options are available in clinical practice. Access planning should include comprehensive assessment, with attention to patient participation in the planning and selection process. Careful consideration should be given to long-term access needs and preservation of access sites. IMPLICATIONS FOR NURSING PRACTICE: Oncology nurses are uniquely suited to perform a key role in VAD planning and placement. With knowledge of infusion therapy, anatomy and physiology, device options, and community resources, nurses can be key leaders in preserving vascular access and improving the safety and comfort of infusion therapy. KEY WORDS: Vascular access device, venous anatomy and physiology, power injection, assessment.

V

ASCULAR access devices (VADs) were developed to ease the administration of infusion therapy for both clinicians and patients. To a great degree, these devices have allowed individuals to safely receive intensive infusion therapy, to receive increasing

Gail Egan Sansivero, MS, ANP: Instructor, Department of Radiology, Division of Vascular and Interventional Radiology, Albany Medical College, Albany, NY; Nurse Practitioner, Division of Vascular and Interventional Radiology, Community Care Physicians, PC, Latham, NY. Address correspondence to Gail Egan Sansivero, MS, ANP, Albany Medical College, Department of Radiology, MC-113, 47 New Scotland Ave, Albany, NY 12208. e-mail: [email protected] Ó 2010 Elsevier Inc. All rights reserved. 0749-2081/10/2602-$32.00/0. doi:10.1016/j.soncn.2010.02.006

complex therapies in the home, and to preserve vascular access. Their accurate use requires a comprehensive approach to assessment, device placement planning and use, potential complication management, and removal. There are many factors that influence the selection and placement of a central vascular access device (CVAD) in a given clinical situation. For clarity, these factors can be divided into four categories: 1) patient characteristics and preference; 2) history and co-morbidities; 3) infusion needs; and 4) device options. A partnership between the clinician and patient is critical in achieving the optimal outcome of placing the right device, at the right time, in the right location. A consultation visit will allow the clinician to assess the overall clinical situation, offer the patient options, and make a device placement and management plan.

FEATURES AND SELECTION OF VADS

(See Appendix 1 for a sample vascular access consult.)

PATIENT CHARACTERISTICS Considering VAD selection from the perspective of the patient is a critical step that is often ignored. Patients must be given the opportunity to evaluate device options in view of their lifestyle and ability, and willingness to perform maintenance. There are few studies that examine patient preference for type of VAD. Dearborn et al1 evaluated nurse and patient satisfaction with tunneled catheters and ports in an outpatient oncology setting. Using a self-report strategy, they reported on catheter dysfunction, global satisfaction, and potential perceived benefits of having a VAD. Eighty-five adult patients responded, with the majority satisfied with their devices despite intermittent performance problems. The study was limited in sample size and patients were typically not experienced with other VAD options. Chernecky2 surveyed a convenience sample of 24 adult oncology patients with implanted ports who also had experience with at least one chemotherapy treatment delivered via peripheral cannula. Overall patients were more satisfied with receiving treatment utilizing an implanted port than a peripheral venipuncture. Subjects most frequently reported that their satisfaction was related to decreased pain, fewer needlesticks, and more efficient venous sampling. Recently, Johansson et al3 queried 32 adult patients with leukemia about their satisfaction with either a tunneled central venous catheter (CVC) or an implanted port.3 Data were collected on the day after device placement, 3 weeks following placement, and 12 weeks after placement or upon device removal. Patients who experienced bleeding complications were more likely to report the CVAD was unpleasant. Overall, patients with implanted ports reported less impact on their daily life than a tunneled CVC. Although many different devices may meet the infusion needs of a given individual, the patient may have a preference for a particular VAD. For example, a life-long total parenteral nutrition (TPN)-dependent patient may prefer an implanted port to a tunneled VAD. While the clinician may recommend an external device in a setting in which daily infusions are needed, the patient may elect to have an implanted device that will allow several

89

hours of ‘‘access-free’’ time each day. In any case, the advantages and disadvantages of each device should be discussed. Demonstration of sample devices is helpful in assisting the patient to understand exactly what the device looks like and how it will impact daily life. The initial interaction should include an assessment of the patient’s understanding of their diagnosis, the prescribed therapy including duration, risks, benefits, and operational issues (eg, use of pumps, etc). The inclusion of a family member or friend is ideal to provide moral support and additional assistance in device care and infusion therapy. The ability of the patient to provide self-care is an important aspect of the initial assessment. Patients must be able to see and reach their device and should be asked for their preference for the site of the device. Many individuals prefer to have the upper extremity device placed in the non-dominant arm to facilitate self-care. Upper extremity sites should be high enough from the antecubital fossa so that range of motion is not impeded by the device or extension sets. Exit sites on the chest should be placed low enough so that the patient can see the site without the aid of a mirror. Consideration needs to be given to contact from seat belts, bra straps, and the patient should be asked about typical clothing styles so that the device site can be hidden if desired. The patient’s typical activities, including occupational and recreational pursuits, should be assessed because modifications of the device site, securement, and maintenance may be necessary for the patient to engage in desired activities. The site selected can be labeled with a surgical marker before device insertion (Fig. 1). In confused or mentally incapacitated adults or small children, creative strategies for siting devices may reduce accidental device migration. A device may be tunneled in a retrograde fashion from an internal jugular vein site, across the shoulder to a location just above the scapula. This ‘‘out of sight, out of mind’’ strategy may be effective in reducing an incapacitated patient’s awareness of the device’s presence, and reducing inadvertent manipulation.

HISTORY AND CO-MORBIDITIES Patients should be queried about past VAD use, including type, performance, complications, satisfaction, etc. Many patients may not recall use of a shortterm device, though it can be assumed that those who

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G.E. SANSIVERO

FIGURE 2. J-tip guidewire entrapped in inferior vena cava filter.

FIGURE 1. Selecting and marking a VAD exit site befor device placement.

have undergone major surgical procedures will have had a CVAD. Patients should be specifically questioned about surgical interventions that may impact the placement and use of a VAD, such as vein harvesting, intravenous stent placement, and the presence of other devices, such as defibrillators or pacemakers. Patients should also be asked about the presence of inferior vena cava (IVC) filters. Advancing guidewires, especially J-tip guidewires, should be done with caution in patients with IVC filters because wires can be inadvertently trapped in the filter (Fig. 2). In patients with IVC filters, a straight-tip guidewire should be used for VAD placement and care should be taken not to advance the guidewire to the level of the filter. There are a number of co-morbidities that can affect device selection, placement, and wound healing (eg, diabetes, steroid use, edema, and lymphedema). Additional measures to promote wound healing may be taken in these patients, such as a longer time before sutures are removed, use of alternative securement devices, and use of special dressing materials. Material allergies that impact placement of a VAD may include latex sensitivity, sensitivity to adhesive materials, and allergy to skin prep solutions or topical and local anesthetics. The clini-

cian should confirm that all components of a VAD kit and materials, including gloves and ultrasound transducer sheaths, are latex-free if indicated. Although chlorhexidine is the preferred skin preparation solution, patients with sensitivity can be prepped with isopropyl alcohol and povidone iodine.4,5 Patients with a sensitivity to lidocaine can receive a local anesthetic with novacaine or normal saline, or a topical agent. Current evidence suggests that prophylactic antibiotic use before device placement is not warranted.6

THE PHYSICAL EXAM The physical examination is an important but often overlooked portion of vascular access assessment. Overall skin turgor should be assessed, with an emphasis on skin condition at the planned device site(s). Presence of any skin lesions (including ecchymoses), scars, edema, or grafts should be noted. The presence and location of any collateral veins should be noted. Prominent superficial veins in the area of planned VAD placement may indicate neighboring or central vein stenosis (Fig. 3). The ultrasound appearance of a very large target vein in a small individual may also represent venous dilation from a distal stenosis or occlusion. At no time should the clinician assume that a large, patent target vein indicates that a VAD can be advanced to its desired tip location. A focused examination should be made of the intended puncture site. Palpation of the site for tortuous or sclerosed and scarred veins should be performed. The examiner should assess for the presence of other medical devices in the target

FEATURES AND SELECTION OF VADS

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FIGURE 3. Superficial enlarged collateral veins across chest in a patient with complete SVC occlusion. area. These include pacemakers, automatic implantable cardioverter defibrillators (AICDs), tracheostomies, and other VADs. Although these do not preclude neighboring device placement, they do require the clinician to make a thorough plan to appropriately place the new VAD. The clinician should next assess the patient’s ability to be positioned for device placement. Range of motion in the neck, upper extremity, and shoulder may be assessed if the arm or neck and chest area are used for access. Contractures and decreased range of motion may make positioning for placement challenging, and may impact on the patient’s ability to perform selfcare. Comorbid conditions that may impact on positioning include arthritis, dyspnea, back or neck conditions, and obesity. Pain medications, oxygen, and supportive devices may be used to ameliorate these conditions. Modifications in the placement plan may be made to accommodate these challenges, and in severe cases may warrant a change in device selection.

INFUSION NEEDS Both the short- and long-term needs of any given patient should be evaluated with each consultation encounter. It is imperative that vascular access be preserved, and that the limited number of access sites available is considered in access planning. For example, a patient with pancreatic cancer in the initial stages of treatment may only need a single lumen catheter. In the setting of advanced disease, however, additional infu-

sion capability may be necessary and placement of a dual lumen implanted port will provide both initial infusion capability, plus long- term access options, while using only one access site. While some patients may need a VAD for infusion of a single agent, it is common for multiple infusions to be given sequentially or simultaneously. The primary infusions (eg, an antineoplastic agent) plus associated agents (eg, anti-emetics, steroids, IV fluids, antibiotics) should be factored into the access plan. Any vesicant or irritant properties of infusates should be identified, with provisions made for assessment of device patency and security. Infusion rates and compatibilities of all infusates should be known, and provisions made for sequencing of incompatible infusions or the use of a multi-lumen VAD. Maximum infusion rates are typically available on device packaging and on the manufacturer’s websites. Stability of infusates is important to consider, particularly in the home setting when infusion pumps are loaded for infusions that may last a week. Provisions may need to be made for cassette or reservoir changes. The duration of intended therapy should be calculated, with the goal of delivering the entire treatment course with one device.

SPECIAL CONSIDERATIONS FOR THE YOUNG PATIENT Young patients have special needs that should be addressed during the assessment phase of vascular access consultation. Concerns about body image and self-esteem should be a part of

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the routine access assessment. Teenagers may be particularly concerned about device concealment and device location. They may prefer a device be placed in the upper extremity rather than the chest area, or to have a chest exit site located low enough so that the device may not be seen, even with limited clothing. In infants and neonates, alternate sites may be considered for device placement. These sites include the saphenous vein, the temporal veins (especially in infants), and the femoral veins.7 The small target veins in infants and neonates can make cannulation challenging, while larger veins are deeper and may not be visible or palpable. Use of the modified Seldinger technique, coupled with imaging technology (ultrasound, transillumination), may assist in cannulation of these vessels. Children and infants may require creative approaches to device maintenance. Very small securement devices and dressing materials may be used to stabilize devices. Additional measures to avoid accidental device withdrawal and migration may be implemented as well. These may include the use of gauze wraps or ‘‘Ace’’ type wraps over an extremity. Materials that are comfortable for use should be selected.

sisting of collagen and elastic fibers, sympathetic nerves that maintain vasomotor tone (venous pressure), and blood vessels that nourish the vein. Most intravenous cannulas lie parallel to the vessel. Devices are much more likely to have contact with the vein (and the intima) in a smaller caliber vessel. In a larger vessel, such as the superior vena cava (SVC), the catheter is less likely to be in direct contact with the vessel wall. Forauer and Theoharis10 studied the impact of CVCs on vein walls in six patients post mortem. All patients demonstrated local intima injury with endothelial denudation and a layer of adherent thrombus. In patients who had VADs in place for longer than 90 days, vein wall thickening was seen along the entire intravascular course of the device in addition to focal areas of catheter attachment to the vein wall. In the upper extremity, the basilic, brachial, or cephalic veins may be used for VAD placement (Fig. 4). The basilic vein is the preferred choice because it is typically the largest upper extremity vein, follows a fairly straightforward pathway to the subclavian vein, and is not in close proximity to neighboring arteries. Brachial veins accompany

VEIN PHYSIOLOGY AND INTRAVENOUS THERAPY The vein wall is composed of three layers.8 The innermost layer is the tunica intima; it is composed of a single layer of endothelial cells. This layer is easily damaged by venipuncture and VAD placement. If the intima is disrupted, an inflammatory response is initiated and with a rougher surface available for platelet aggregation a thrombus can occur. Thus, it is critical that the intima be preserved by limiting the number and type of punctures as well as the infusion of irritating solutions that may also damage this layer. The middle layer of the vein wall is the tunica media. This layer contains elastic and smooth muscle fibers that allow the vein to constrict or expand in response to changes in blood pressure and flow. Anxiety, temperature changes, and chemical or mechanical irritation may also cause the vein to constrict or dilate.9 These changes may enhance or impede vessel cannulation because the vein feels tougher due to less compliance and greater stiffness. The outermost layer of the vein wall is the tunica adventitia. It is composed of connective tissue con-

FIGURE 4. Veins of the upper extremity. (Illustration courtesy of M. Ciarmiello.)

FEATURES AND SELECTION OF VADS

the brachial artery in pairs and are known as vena comitans or ‘‘companions of the arteries.’’ The brachial veins drain into the axillary vein, occasionally joining the basilica vein. When placing VADs near the brachial vein, clinicians must carefully avoid inadvertent puncture of the brachial artery, or irritation of the brachial nerve, which resides in the same bundle. If a port is placed via the brachial vein approach, the port pocket must be carefully situated to avoid arterial and nerve damage. The cephalic vein is the smallest of the upper extremity veins and is located lateral to the biceps. It makes a tighter downward pathway to the subclavian vein just past the shoulder, and this, coupled with its smaller size, makes it a poorer choice for VAD placement in most patients. In the chest, the subclavian vein is often used for VAD placement. The subclavian is a continuation of the axillary vein and it joins the internal jugular vein to form the brachiocephalic vein, lying anteriorally and inferiorally to the subclavian artery (Fig. 5). Devices placed via the subclavian vein must enter laterally so that the device resides within the vein before passing through the costoclavicular space. Doing so diminishes the risk of ‘‘pinch off’’ syndrome, which may result in catheter dysfunction and embolization. The brachiocephalic veins (also known as the innominate veins) represent the union of the

internal jugular veins and the subclavian veins. The right brachiocephalic vein is substantially shorter (2.5 cm) than the left (6 cm). The brachiocephalic veins join to form the SVC. The major source of venous drainage for the upper body is the SVC, which ends in the right atrium and is typically around 7cm in length. The azygos vein is a tributary of the SVC, and often enlarges in the setting of SVC stenosis or occlusion. In the neck, both the internal and external jugular veins are available for VAD placement (Fig. 6). The external jugular drains primarily the scalp and face and descends superficially from the head to the thorax. It ends in the subclavian vein. It is smaller and more tortuous than the internal jugular vein, and therefore should not be the first choice for VAD placement. The internal jugular vein drains the brain and superficial and deep portions of the face and neck. It descends into the neck in the carotid sheath, typically anterior to and lateral to the carotid artery. It joins the subclavian vein posteriorly to the sternal end of the clavicle, forming the brachiocephalic vein. Because of its size and relatively straight pathway to the brachiocephalic veins, the internal jugular vein is the first choice for VAD placement in the neck. In the setting of SVC occlusion, the IVC may be used for VAD placement. Formed by the confluence of the iliac veins, the IVC carries blood from

internal jugular vein external jugular vein

internal jugular vein external jugular vein

right brachiocephalic vein

left subclavian vein internal thoracic vein left brachiocephalic vein

internal thoracic vein right superior intercostal vein superior vena cava azygos vein right pericardiophrenic vein

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left superior intercostal vein

left pericardiophrenic vein accessory hemiazygos vein hemiazygos vein

inferior vena cava

FIGURE 5. Veins of the chest. (Illustration courtesy of M. Ciarmiello.)

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FIGURE 6. Veins of the neck. (Illustration courtesy of M. Ciarmiello.) all organs below the diaphragm back to the heart. The IVC may be accessed directly (via a translumbar approach) or indirectly (via the common femoral veins [CFVs] or hepatic vein, known as the transhepatic approach) for VAD placement.

TIP LOCATION Essential to the understanding of central venous anatomy and catheter tip position is that catheter tips are not fixed. Devices move with inspiration and expiration, with change in patient position and with upper extremity movement.11 The tip of a CVAD is typically positioned in the distal third of the SVC (Fig. 7). Yet the optimal tip position of CVCs remains a complex and controversial subject despite publications of numerous professional organizations.11 The US Food and Drug Administration, the Oncology Nursing Society, the National Association of Vascular Access Networks (now the Association for Vascular Access), and the Infusion Nurses Society have all published statements that catheter tips should not reside in the right atrium. In addition, the American Society for Parenteral and Enteral Nutrition recommends a CVAD used for parenteral nutrition be placed with its tip in the SVC adjacent to the right atrium.12 There is some evidence that larger catheters, such as hemodialysis and apheresis catheters, require a catheter tip position in the upper right atrium for maximum performance.11 Unfortunately, there is

limited consensus on determining the exact location of a VAD tip using chest x-ray or fluoroscopy. The distal SVC and the atriocaval junction are only estimated on chest x-ray because they are not specifically visualized using this modality. Surrogate landmarks, such as the caudad margins of the clavicles, the third intercostal space, or the tracheobronchial angle, are used to estimate catheter tip position. It is particularly difficult to determine catheter tip location using portable chest x-rays, which is often utilized in critically ill patients.13 The radiographic borders of the SVC and SVC/atrial junction have not been well-defined. Thus, chest x-ray interpretation

FIGURE 7. Peripherally inserted central catheter tip located at the atriocaval junction. (Image courtesy of T.M. Vesely.)

FEATURES AND SELECTION OF VADS

of CVAD placement is subject to significant variability. Venograms are more accurate in identifying venous anatomy and potential pathology. However, they require venous access, which may be a peripheral cannula, and the administration of IV contrast to opacify vessels. Routine venogram for the purposes of CVAD placement is not necessary and exposes the patient to unnecessary radiation and contrast. Venography is useful in patients with a history of central vein stenosis or thrombus, or in complicated placement situations. Numerous studies have evaluated computed tomography (CT) scans, CT angiograms, and magnetic resonance imaging relative to catheter placement and tip location.13-15 DeChicco et al16 studied 138 CVC tip locations in patients with peripherally inserted central catheters (PICCs), implanted ports, and tunneled catheters placed for parenteral nutrition or chemotherapy. Evaluating pre-existing VADs, the authors noted a higher incidence of tip malposition in PICCs (34%) as compared with tunneled VADs or implanted ports (9%). The authors attribute this difference to a higher likelihood of accidental PICC dislodgement because of suture or securement device failure, when compared with devices secured by a Dacron cuff or subcutaneous pocket. Given the relationship between catheter-related thrombosis and catheter tip position, the authors recommend verification of accurate tip placement in all patients presenting with a CVAD. In a study of 437 adult cancer patients, Caers et al17 compared tip placement of implanted ports, with complications including dysfunction, thrombosis, and infection. Catheter tips positioned in the brachiocephalic vein or cranial portion of the SVC were associated with a higher risk of catheter-related thrombosis. Chaturvedi et al18 noted a higher incidence of catheter tip malposition in pediatric patients when compared with adult patients. In 200 pediatric patients ranging in age from 1 to 15 years, devices were placed in the upper extremity with tip location confirmed radiographically. The catheter tips were adequately positioned in only 49% of the patients. The most common incorrect tip locations were the ipsilateral internal jugular vein or subclavian vein. Children ages 1 to 5 years were most likely to have catheter tip malpositions as compared with their older cohorts. New developments in tip verification technology are currently being tested in clinical prac-

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tice. Also known as location or navigation systems, devices in development include EKGbased19 and electromagnetic-based systems.20 Electromagnetic systems use an electromagnetic signal that is typically transmitted to a monitor via a sensing device attached to or inserted into the VAD. An external sensor or ‘‘wand’’ type device is then tracked over the patient’s chest to obtain a signal indicating the catheter tip location. These devices transmit a signal that indicates the VAD’s direction and location in relation to anatomic landmarks. EKG-based systems use the VAD as an intracavitary electrode, connected to a transducer, that detects changes in the P wave, which reflects the catheter tip location.19 As the catheter moves from the SVC into the right atrium, changes in height of the P wave indicate the catheter tip position. EKG-based systems have been tested extensively. In a study of 100 adult patients, Schummer et al20 noted a significant increase in P wave amplitude when catheter tips were located at the pericardial reflection, rather than at the entrance to the right atrium. Because EKG-based systems rely on changes in P wave amplitude, their utility may be limited in patients with rhythm disturbances such as atrial fibrillation and severe tachycardia, and in patients with pacemaker-driven rhythms. The electromagnetic systems and EKG are minimally invasive options for tip verification that may reduce radiation exposure to patients by eliminating chest x-ray or fluoroscopy. In addition, there is no delay between device placement and tip verification, so infusion therapy may begin immediately after device placement. Further testing is needed to validate these approaches to catheter tip verification.

DEVICE OPTIONS Currently, no standard nomenclature exists for VADs. Devices may be referred to by characteristics (‘‘triple lumen’’), by location (‘‘femoral line’’), brand (‘‘Hickman’’), or category (‘‘PICC’’). Each of these strategies is problematic. A particular device may be placed in almost any location. The number of lumens gives us little information about the device. A brand name is often used to refer to an entire device category, and may be inaccurate. The resulting confusion among clinicians and patients alike is

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understandable. This section will refer to devices by their overall generic characteristics. Non-Tunneled, Non-Cuffed Devices Representing the largest market share of CVADs in the United States, non-tunneled, non-cuffed devices may include catheters typically used in critical care, as well as PICCs. These devices are inserted via a percutaneous approach, with a catheter tip residing in a central location. Their entry and exit sites are one and the same. Available in lumen configurations ranging from one to five, these devices are suitable for a variety of infusion needs. Often referred to as ‘‘temporary’’ catheters, these devices may have an extended dwell time in some clinical situations. For example, a PICC may remain in place for several years if needed. A device such as a Hohn (BARD Access Systems, Salt Lake City, UT) may also be used for several months, regardless of the site of care delivery. It is typically the overall clinical condition of the patient that will determine dwell time, rather than the device characteristics. The exception is devices in the critical care environment, where the risk of infection increases dramatically after 5 days of placement. Devices coated with chlorhexidine/sulfadiazine or rifampin/minocycline have significantly lower infection rates in the critical care population.21 There is currently no evidence to support the use of other VADs with coatings. PICCs have often been chosen when the duration of therapy is estimated to be more than 2 weeks. Basing device selection on this criteria alone, however, does not take into account infusate characteristics, which may be inappropriate for short-term peripheral cannula use.7 Tunneled and Cuffed Devices Frequently known as ‘‘Hickmans,’’ tunneled and cuffed catheters have been available since 1969. They are often used in the treatment of hematologic malignancies, especially in bone marrow transplant settings and in the administration of long-term TPN in the home. Available in one to three lumen configurations, these devices offer a durable option for patients who may require therapy for a prolonged period. Because the device’s exit site is remote from the vein insertion site, tunneled cuffed catheters are quite stable. The location of the exit site can be manipulated to accommodate patient preference and comfort. Subcutaneous tissue grows into the Dacron cuff over a period of 4 to 6 weeks,

providing added stability and, it is theorized, additional protection from device-related infection. Tunneled cuffed catheters are typically comfortable to use once healed because any sampling or infusions are performed simply by securing a luer lock connection. Implanted Ports First tested in 1982, implanted ports have become a standard VAD for patients with cancer, particularly those who require intermittent therapy. Implanted ports offer an advantage when compared with other devices of very limited maintenance because of their completely implanted design. As such, there are also few if any activity limitations for patients whose ports are accessed with a non-coring needle. Ports can be placed via any approach, with the internal jugular or subclavian veins generally chosen first. For patients with tracheostomies, laryngectomies, or other neck or chest devices/pathology, the portal body can be placed in the upper extremity and the catheter threaded to a central tip location from a basilic, brachial, or cephalic vein. Placement in the upper extremity is often preferred by adolescents who may perceive that there is less body image distortion with this approach, and that the device may more easily be concealed. Regardless of port pocket and access site, placement of upper extremity ports compare favorably in terms of complication profile and outcomes with ports placed in the chest.22,23 The timing of implanted port placement should be coordinated with the patient’s therapy so that the site has time to heal before use. (If necessary,

FIGURE 8. Implanted port with non-healing site. Note eschar at the site.

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TABLE 1. Advantages and Disadvantages of VADs Type of Device Non-tunneled, non- cuff device

Tunneled cuffed VAD

Implanted port

Advantages

Disadvantages

Rapid insertion Easy to access Available in multiple lumen configurations (1-5) May be power injectable Easy and rapid removal Limited long-term scarring at site Useful for multiple infusions, dialysis, apheresis No discomfort with use once placed Moderately easy to place Available in multiple lumen configurations Stable when compared with non-tunneled devices May be repairable if damaged Long dwell times in many consumers No discomfort with use once placed Useful for multiple infusions, including dialysis and apheresis (depending on device size) Long dwell time/durability Limited maintenance Limited body image distortion (cosmetic advantage) Little if any activity limitations

ports can be accessed for immediate use in the operating room or interventional radiology suite). Ports should not be placed during the patient’s nadir, when infectious complications are more likely to occur. In addition, patients receiving bevacizumab are at higher risk of developing wound dehiscence resulting in port removal than patients who do not, particularly if bevacizumab was given within 10 days prior to port placement (Fig. 8).24 Bevacizumab has a half-life of 20 days, and the manufacturer recommends that the drug be held for 4 weeks before and after any surgical procedure. However, there are no guidelines for treatment timing for minimally invasive procedures.25 Further studies are needed to evaluate the optimal timing of VAD placement in patients receiving antiVEGF therapy. Table 1 summarizes the advantages and disadvantages of the various access devices.

Requires stabilization with sutures or securement device Less stable than tunneled devices Requires frequent maintenance External location, less cosmetically acceptable Typically shorter dwell time than tunneled or implanted devices Some activity restrictions Requires frequent maintenance External location less cosmetically acceptable Some activity restrictions

Most invasive insertion & removal procedure Some discomfort with access Requires training to access Requires special needle to access Limited to dual lumen configuration

In the setting of SVC stenosis, consideration can be given to recanalization using interventional radiology techniques. If the SVC can be crossed with a guidewire under fluoroscopic guidance, an angioplasty balloon can be advanced to the point of stenosis and inflated (Fig. 9). When the balloon is deflated, a contrast injection is performed to evaluate for efficacy. In the setting of long-term or chronic SVC stenosis, an intravascular stent

VAD PLACEMENT IN CHALLENGING SITUATIONS VAD placement can be challenging in patients with limited peripheral access and central vein occlusion, as well as those with profound co-morbidities, such as morbid obesity. However, use of ‘‘unconventional access’’ techniques can allow these patients to attain a fully functional VAD.

FIGURE 9. Angioplasty balloon inflated in the right brachiocephalic vein. Note the ‘‘waist’’ on the balloon, which reflects an area of venous stenosis.

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FIGURE 10. Intravascular stent within the superior vena cava. Apheresis catheter is placed from the right internal jugular vein and advanced through the stent.

can be placed to maintain patency (Fig. 10). A CVAD can then be inserted through the stent. The azygos vein often becomes dilated in the setting of SVC occlusion. The azygos vein ascends from the abdomen and arches anteriorally to enter the posterior wall of the SVC. It is a collateral vein that enlarges in the setting of SVC occlusion. While not typically used for CVC tip placement, the azygos vein offers an alternative before other sites (such as direct IVC placement) are entertained. The azygos vein can be assessed with magnetic resonance venography (MRV) or standard venography. When using any collateral vein for access, clinicians should be cognizant of the potential complications of occlusion of a dominant collateral, leading to venous outflow obstruction.26 Translumbar venous access is another approach to establish access both in children and adults in the setting of SVC occlusion. The patient is placed in the supine position, and a guidewire is advanced from the CFV into the IVC to be used as a marker and secured. The patient is then repositioned into the prone position, and the IVC accessed under fluoroscopy using the pre-existing guidewire to locate the IVC. Standard procedures are then followed for tunneling and exit site formation. Port pockets should be placed over the iliac crest or anterior ribs so that they are easily palpable and stabilized for access. Transhepatic access is an alternative approach into the IVC. It can be used in the setting of SVC occlusion, and in patients with intrarenal vena cava occlusion. Typically, the middle hepatic vein is accessed and a guidewire then threaded into the IVC, followed by standard VAD placement tech-

niques. The tunnel is generally formed superior and lateral to the entry site. A more posterior approach may be used in patients in whom accidental withdrawal is a concern. Because the liver is traversed in this approach, any coagulopathy should be corrected before placement. Interval growth in children may result in catheter tip displacement, prompting clinicians to assess tip placement using serial plain films at selected intervals. The CFV may be used for VAD placement in both acute and chronic settings. When used for short-term access, the femoral vein is associated with a higher rate of catheter-related blood stream infections (CR-BSIs) than other sites. However, there is little data on the use of long-term tunneled catheters or implanted ports via the CFV. In our experience, these devices may have substantial longevity in patients with cancer, chronic kidney disease, and short bowel syndrome. The CFV is accessed using standard techniques. The device exit site may be on the thigh, usually in a lateral area for ease of access or tunneled in a retrograde fashion up the abdomen.

POWER INJECTION OF CVADS New products on the vascular access market have allowed clinicians to utilize indwelling CVADs for contrast injection using high infusion rates over a short period of time. Manufacturers have responded by developing VADs that can sustain the pressure and infusion rates generated by power injectors. The ability to power inject through VADs can potentially decrease patient discomfort, reduce injection times, and improve CT imaging quality. First introduced in 2003, these devices can withstand injection rates up to 5 ml/second. There are two types of PICCs, regular and power. Only power PICCs (usually purple in color) should be used for power injection for safety reasons. The reader is referred elsewhere for additional studies related to power injections via central lines.27-33

CONCLUSION CVADs offer patients the opportunity to receive complex therapies in a safe and effective manner. A wide variety of device choices means that devices can be specifically selected to meet patient preferences and deliver therapy comfortably. Even in the most complex clinical situation, accurate assessment coupled with expert placement can result in durable access outcomes. Despite

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more than 40 years of clinical use, further research is needed to evaluate optimal device

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maintenance strategies and to develop safer and more comfortable devices.

REFERENCES 1. Dearborn P, DeMuth JS, Requarth AB, et al. Nurse and patient satisfaction with three types of venous access devices. Oncol Nurs Forum 1997;24:34-40. 2. Chernecky C. Satisfaction versus dissatisfaction with venous access devices in outpatient oncology: a pilot study. Oncol Nurs Forum 2001;28:1613-1616. 3. Johansson E, Engervall P, Bjorvell H, et al. Patients’ perceptions of having a central venous catheter or a totally implantable subcutaneous port system-results from a randomized study in acute leukaemia. Support Care Cancer 2009;17:137-143. 4. Posa PJ, Harrison D, Vollman KM. Elimination of Central line-associated blood stream infections: application of the evidence. AACN Adv Crit Care 2006;17:446-454. 5. Maki DG, Kluger DM, Crnich CJ. The risk of bloodstream infection in adults with different intravascular devices: a systematic review of 200 published prospective studies. Mayo Clin Proc 2006;81:1159-1171. 6. vandeWetering MD, vanWoensel JB, Kremer LC, et al. Prophylactic antibiotics for preventing early gram positive central venous catheter infections in oncology patients: a Cochrane systematic review. Cancer Treat Rev 2005;31:186-196. 7. Pettit J. Technological advances for PICC placement and management. Adv Neonatal Care 2007;7:122-131. 8. Macklin D, Chernecky C. IV Therapy. St. Louis, MO: Elsevier; 2004. 9. Hadaway LC. Anatomy and physiology related to intravenous therapy. In: Terry J, Barnowski L, Onsway RA, Hedrick C, eds. Intravenous therapy: clinical principles and practice. Philadelphia, PA: Saunders; 1995: pp. 81-110. 10. Forauer AR, Theoharis C. Histologic changes in the human vein wall adjacent to indwelling central venous catheters. J Vasc Interv Radiol 2003;14:1163-1168. 11. Vesely TM. Central venous catheter tip location: a continuing controversy. J Vasc Interv Radiol 2003;14:527-534. 12. Steiger E. HPEN Working Group. Consensus statements regarding optimal management of home parenteral nutrition (HPN) access. J Parenter Enteral Nutr 2006;30(Suppl):S94-S95. 13. Aslamy Z, Dewald CL, Heffner JE. MRI of central venous anatomy: implications for central venous catheter insertion. Chest 1998;114:820-826. 14. Baskin KM, Jimenez RM, Cahill AM, et al. Cavoatrial junction and central venous anatomy: implications for central venous access tip position. J Vasc Interv Radiol 2008;19:359-365. 15. Mahlon MA, Yoon HC. CT angiography of the superior vena cava: normative values and implications for central venous catheter position. J Vasc Interv Radiol 2007;18:1106-1110. 16. DeChicco R, Seidner DL, Brun C, et al. Tip position of long-term central venous access devices used for parenteral nutrition. J Parenter Enteral Nutr 2007;31:382-387. 17. Caers J, Fontaine C, Vinh-Hung V, et al. Catheter tip position as a risk factor for thrombosis associated with the use of subcutaneous infusion ports. Support Care Cancer 2005;13:325-331.

18. Chaturvedi A, Bithal PK, Dash H, et al. Catheter malplacement during central venous cannulation through arm veins in pediatric patients. J Neurosurg Anesthesiol 2003;15: 170-175. 19. Pittiruti M, Scoppettuolo G, LaGreca A, et al. The EKG method for positioning the tips of PICCs: results from two preliminary studies. J Assoc Vascular Access 2008;13:179-186. 20. Schummer W, Schummer C, Muller A, et al. ECG-guided central venous catheter positioning: does it detect the pericardial reflection rather than the right atrium? Eur J Anaesthesiol 2004;21:600-605. 21. Maki DG, Kluger DM, Crnich CJ. The risk of bloodstream infection in adults with different intravascular devices: a systematic review of 200 published prospective studies. Mayo Clin Proc 2006;81:1159-1171. 22. Kawamura J, Nagayama S, Nomura A, et al. Long-term outcomes of peripheral arm ports implanted in patients with colorectal cancer. Int J Clin Oncol 2008;13:349-354. 23. Bodnar LJ, Nosher JL, Patel KM, et al. Peripheral venous access ports: outcomes analysis in 109 patients. Cardiovasc Intervent Radiol 2000;23:187-193. 24. Zawacki WJ, Walker G, DeVasher E, et al. Wound dehiscence or failure to heal following venous access port placement in patients receiving bevacizumab therapy. J Vasc Interv Radiol 2009;20:624-627. 25. Almhanna K, Pelley RJ, Budd GT, et al. Subcutaneous implantable venous access device erosion through the skin in patients treated with anti-vascula endothelial growth factor therapy. A case series. Anticancer Drugs 2008;19:217-219. 26. Weeks SM. Unconventional venous access. Tech Vasc Interv Radiol 2002;5:114-120. 27. Federle MP, Chang PJ, Confer S, et al. Frequency and effects of extravasation of ionic and non-ionic contrast media during rapid bolus injection. Radiology 1998;206:637-640. 28. Angle JF, Matsumoto AH, Skaleak TC, et al. Flow characteristics of peripherally inserted central catheters. J Vasc Interv Radiol 1997;8:569-577. 29. Williamson EE, Mckinney JM. Assessing the adequacy of peripherally inserted central catheters for power injection of intravenous contrast agents for CT. J Comput Assist Tomogr 2001;25:932-937. 30. Salis AI, Exlavea A, Johnson MS, et al. Maximal flow rates possible during power injection through currently available PICCs: an in vitro study. J Vasc Interv Radiol 2004;15:275-281. 31. Ruess L, Bulas DI, Rivera O, et al. In-line pressures generated in small-bore central venous catheters during power injection of CT contrast media. Radiology 1997;203:625-629. 32. Rigsby CK, Gasher R, Seshadri R, et al. Safety and efficacy of pressure-limited power injection of iodinated contrast medium through central lines in children. Am J Roentgenol 2007;188:726-732. 33. Donnelly LF, Dickerson J, Racadio JM. Is hand injection of central venous catheters for contrast-enhanced CT safe in children? Am J Radiol 2007;189:1530-1532.

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Appendix 1

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2.5 ANCC/AACN CONTACT HOURS

Fluid balance Critical and aspects of ICU care

Critically ill patients are at great risk for volume depletion that may be secondary to internal and external fluid losses. Daily fluid balance assessments may be inaccurate, as total volume losses aren’t always recognized or measurable. Hypovolemia can progress from a state of mild dehydration to severe and profound fluid loss that may lead to shock and end organ failure if not treated appropriately. Despite the daily recording of a positive or negative fluid balance, patients’ clinical status must be addressed in relation to evaluating the severity of their hypovolemic state. These patients can present with symptoms that may be acute, chronic, or acute on chronic. According to experts, “A patient may be in shock despite having a normal heart rate and blood pressure.”1 That statement truly emphasizes that a critically ill patient can have normal hemodynamic parameters; however, end organ perfusion may be compromised. Without adequate fluid resuscitation, tissue ischemia worsens, and chances for an optimal recovery decrease.

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l Nursing2008Critical Care l Volume 3, Number 2

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resuscitation By Wendy J. Stevens, CRNP, MSN

www.nursing2008criticalcare.com

March l Nursing2008Critical Care l

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Fluid balance and resuscitation

The circulating volFluid compartments by gender ume in the body is a small percentage comFluid Male Female (80 kg) (70 kg) pared to the overall fluid that the body Total body fluid 0.6 liter or 600 mL/kg = 48 liters 0.5 liter or 500 mL/kg = 35 liters contains. As a result, a Whole blood 66 mL/kg = 5.3 liters 60 mL/kg = 4.2 liters 15% to 20% blood loss Plasma 40 mL/kg = 3.2 liters 36 mL/kg = 2.5 liters has less effect on the circulation than if Red blood cells 26 mL/kg = 2 liters 24 mL/kg = 1.6 liters there is a 30% to 40% (Marino P. 2007) blood loss, which can result in life-threatening circulatory failure.2 Fluid tion include decreased responweights, heights, and lean body siveness, tachycardia with a low resuscitation must not be mass vary. Water makes up the blood pressure, renal failure delayed and treatment goals are largest component of the body along with poor urine output, set in order to guide manageand is present in higher quantiment. Daily physical exams, lab- slow capillary refill, and weak ties in people who have more peripheral pulses. Keep in mind, muscle mass versus fat and is oratory values, and invasive these signs and symptoms may present in higher quantities in monitoring evaluate the effecbe an early clue to an underlyan infant versus an adult. Fat tiveness of adequate fluid resusing acute illness. has a low content of water. A citation. Without restoration of In order to adequately fluid effective circulation, organs and person with minimal muscle resuscitate a patient, it’s importissues become ischemic and mass or a person who’s obese tant to know, if possible, what irreversible damage may ensue. will have a lower percentage of type of fluid has been lost, what body water. As a result, a lean Early recognition types of fluid resuscitation can person will have a higher conThe timing of resuscitation is be used, and the amount and tent of water where substantial critical, as mortality is directly timing of fluid resuscitation. fluid losses may not be well tolrelated to the extent and duraDepending on the patient’s curerated. Infants have a total body tion of organ hypoperfusion of rent condition, a thorough water (TBW) of 80% which puts those in hypovolemic shock.2 account of the history of the them at even greater risk, or Identification of the high-risk present illness, physical exam, even intolerance, of fluid losses patient who may be labeled as a and medical history are imporsecondary to a higher TBW “nonresponder” to initial mantant pieces of information to (compared with an adult).4 agement, may require more obtain which may help guide The percentage of fluid in aggressive fluid resuscitation in treatment. The timing of recoveach body compartment is conorder to avoid irreversible conery, as well as expected benefit, sistent in adults regardless of sequences of shock.3 Patients depends on when treatment is their size; however, the overall who present early with signs of first initiated. TBW content may vary. The body’s fluid compartments can hemodynamic compromise must be divided into TBW and the be monitored in the critical care Physiology of fluid components of blood which are unit. Signs and symptoms of compartments hypovolemia vary depending on Having knowledge of the body’s listed in Fluid compartments by gender. Values are rounded (and the type and duration of fluid fluid composition develops a example, lethargy, conFor to may not equal exact total of loss. greater appreciation for how whole blood amount). Values fusion, anxiety, dry mucous interpret losses in a dehydrated depicted are based on an 80 kg membranes, and tachycardia or hypovolemic patient. All male versus a 70 kg female. The can present in the early stages adults differ in body composi80 kg male typically may have of hypovolemia. Late and more tion and may not require the more lean muscle mass than a ominous signs of volume deplesame amount of fluid because

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70 kg female. Therefore, the TBW is 10% less in a 70 kg female versus an 80 kg male.2 An adult’s TBW content is distributed throughout the extracellular (intravascular and interstitial) and intracellular fluid compartments. Both compartments have the same osmolality, which is determined by the sodium (Na+) salt concentration in the extracellular compartment or the potassium salt concentration within the intracellular compartment. The concentrations of these cations normally stay relatively constant; however, water constantly shifts in order to maintain an equal osmolality between the two compartments.5 Approximately 60% to 65% of TBW exists in the intracellular compartment because more potassium salts exist intracellularly, drawing more fluid than total sodium salts in the extracellular space; however, the osmolality of both compartments remains the same. The remaining 35% to 40% of TBW exists in the extracellular compartment. The extracellular space is defined as the intravascular and interstitial compartments, of which 11% to 12% of the volume is intravascular and the remaining 75% to 80% is in the interstitial space.4 Note that the intravascular space is not a large compartment when compared to the other fluid compartments within the body, which is why it’s very sensitive to volume depletion.

Inside albumin Albumin is an important component of the extracellular fluid compartment. It’s a large protein molecule that exists in highwww.nursing2008criticalcare.com

er concentrations in the interstitial versus intravascular spaces. However, it isn’t able to freely cross the capillary membranes, and therefore helps to maintain adequate colloid pressure to hold water in the intravascular space and retain effective circulating volume. Albumin plays an important role in fluid resuscitation; however, it isn’t often a

coexist in certain clinical conditions as well. A patient who’s relatively hypovolemic may have adequate volume; however, it doesn’t remain or presently exist in the intravascular space. In other words, it isn’t effective circulating volume. Examples include patients with open abdomens, those in septic or distributive shock, and patients

The type of fluid deficit often defines patients’ clinical condition as well as the cause of their hypovolemic state.

first choice secondary to its cost and availability. This is important to take into consideration when deciding which kind of fluid will be most beneficial during initial stages of fluid resuscitation.

Fluid deficits The type of fluid deficit often defines patients’ clinical condition as well as the cause of their hypovolemic state. Patients can present with a fluid deficit secondary to various medical and or environmental conditions. Hypovolemia is best understood when classified as relative secondary to internal fluid shifts as well as insensible losses or absolute secondary to a direct, quantifiable, and usually measurable loss. It’s common that relative and absolute hypovolemic states can

who have high temperatures, profuse diaphoresis, large pulmonary secretions, are ventilator dependent without adequately humidified circuits, or have third space fluid in the interstitial compartment with massive edema. Relative loss that’s due to third spacing may include those with an ileus, intestinal obstruction, compartment syndrome from a fracture, or an intra-abdominal compartment syndrome secondary to a bleed, ascites, or severe acute pancreatitis. Absolute hypovolemia is considered to be measurable fluid loss. Examples include but are not limited to hemorrhage, diarrhea, and high output fistulas (greater than 500 mL/day).6,7

Vital signs Signs and symptoms vary between those who may be

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Fluid balance and resuscitation

mildly dehydrated, profoundly hypovolemic, or in shock and showing signs and symptoms of organ dysfunction. Three ways to evaluate a patient’s fluid status are vital signs, end points, and the use of invasive monitoring. Experts conducted a series of studies to assess the accuracy of vital signs when there is an acute moderate-to-severe blood loss. Moderate blood loss was defined as 450 to 630 mL and severe blood loss was equated to 630 to 1,150 mL, or close to 20% loss of total blood volume.8 They found that supine tachycardia was present in up to 42% of patients with moderate blood loss and only 5% to 24% of patients with severe blood loss. Orthostatics also were checked

in patients that could stand upright. They found that 91% to 100% of patients with severe blood loss had a postural pulse rise of greater or equal to 30 beats per minute (bpm) as well as postural dizziness. A normal increase in heart rate is 10 bpm in healthy individuals.8 Of those with moderate blood loss, 6% to 48% had an increase in pulse rate. Overall, moderate and severe blood loss presented with tachycardia and hypotension in the supine position close to 50% of the time which demonstrates that evaluation of orthostatic vital signs may provide limited information in moderately hypovolemic patients.8 Once blood loss exceeds 30%, hypotension is usually apparent; however, it’s interesting to note that

hemodynamic instability may be a late sign in 50% of hypovolemic patients.9

What’s the end point? Traditionally, measurements of adequate fluid resuscitation include normalization of the heart rate (HR), blood pressure (BP), and urine output (UOP) in both medical and surgical patient populations. Research has shown that despite compensation in shock, ongoing hypoperfusion at the tissue level exists. Three main indicators have been studied to show tissue hypoperfusion at the cellular level and these are lactate levels, mixed venous oxygen saturations (SvO2), and base deficit (greater than -4), which is derived from an arterial blood

Signs and symptoms associated with electrolyte imbalances Hemodynamic effects

Electrolyte

Signs and symptoms

High glucose

• Polyuria, polydipsia, severe dehydration, • Tachycardia secondary to dehydration from high glucose (osmotic diuresis), altered mental status, metabolic hypotension acidosis

Low glucose

• Decreased mental status, seizure

• Dependent on other electrolyte abnormalities

High and low sodium

• Excessive thirst, lethargy, confusion, seizures, coma

• Dependent on other electrolyte abnormalities

High and low potassium

• < 2.5 mEq/liter–diffuse muscle weakness • 2.5 to 3.5–usually asymptomatic, often due to diuresis, magnesium depletion • > 5.5 may be associated with rhabdomyolysis, acidosis, blood transfusions (old blood > 14 days)

• K+ (< 2.5 to 3.0)–prolongation of QT interval but not specific to low potassium levels, (usually other electrolyte deficiencies present), flattened T waves • K+ (> 6.0)–beginning ECG changes, widened QRS, loss of P waves, peaked T waves • K+ 8.0–atrioventricular blocks

Low magnesium

• Associated with secretory diarrhea (not vomiting), hypophosphatemia, altered mentation, seizures, tremors, slurred speech, metabolic acidosis

• Tachyarrhythmia, torsade de pointes

(Kassirer, Hricik, & Cohen 1989, Marino 2007, Martin 1969, Williams, & Rosa 1988)

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Fluid types and compositions Fluid

Na+

Cl-

NaCl (0.9%)

154

154

LR

130

109

4

Normosol

140

98

5

K+

Ca++

Mg++

3 3

pH

Osmolality

5.6

295

Lactate (28 mEqL)

6.4

273

Acetate (27 mEqL)

7.4

295

4.4

278

Buffers

D5W Albumin 5%

130

130

6.4 to 7.4

300

Hetastarch 6%

154

154

5.5

300

5.5

300

Hextend 6% 143 (contains 5 mM/L of glucose)

125

3

5

0.9

Lactate (28 mEqL)

(Gan 1999, Griffith 1986, Halpern et al. 1997)

gas. In two studies of trauma patients, researchers found that despite normalization of vital signs and urine output, close to 80% of patients still had evidence of inadequate tissue perfusion as defined by an elevated lactate level (greater than 4) or decreased SvO2 (less than 60%).10,11 Two other populations that have been studied, assessing end points, have been noncardiac surgical patients and those that are septic.

Lactate and base deficit The relationship between serum lactate levels and hypovolemic shock, as well as its correlation with death in critically ill patients, has been extensively evaluated in several publications from 40 years ago.12 Base deficit has also been evaluated as a measurement of global tissue acidosis since the 1980s.9 Elevated lactate levels are associated with a metabolic acidosis in most cases of hypoperfusion and signify an ongoing oxygen debt at the tissue and cellular level. Both lactate levels and base deficit can be elevated together; www.nursing2008criticalcare.com

however, base deficit can be elevated alone in end stage kidney disease, and in this case, does not indicate a lack of tissue perfusion or an acute process. When comparing elevated lactate levels versus an increased base deficit, an elevated lactate in a hemodynamically unstable patient is associated with a significantly higher mortality rate if not corrected quickly.2

Gastric pH In the last several years, there has also been research done on gastric mucosal pH as a regional end point of resuscitation, as it reflects adequacy of perfusion to the gut. However, this has not yet become a frequent measurement that is used in intensive care units (ICUs) today. It’s considered an adequate regional indicator of resuscitation because blood flow in hypoperfused states isn’t equally distributed, and gastric pH may be the only indicator that perfusion to the splanchnic bed or gut mucosa is still being affected despite a normal lactate and base deficit.13 As a result, clini-

cians have found that despite treatments to improve the traditional end points of HR, BP, UOP, organ tissue oxygenation deficits persist as evidenced by changes in gastric pH.1

Evaluate electrolytes Metabolic derangements and acid/base disorders, as well as their associated signs and symptoms, play a large role when evaluating and treating hypovolemic patients. Laboratory values that are important indicators of volume status are sodium, creatinine, hemoglobin, and lactate. These values may be elevated or decreased depending on their history or disorder that has initially caused their hypovolemic state. (See Signs and symptoms associated with electrolyte imbalances.) A patient’s electrolyte status will determine what type of fluids will be most beneficial during resuscitation. A high sodium level and an elevated creatinine are often initial clues pointing toward dehydration. However, a person’s baseline sodium level may be low in those with heart failure or cir-

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Fluid balance and resuscitation

rhosis, where their effective circulating volume is higher than normal and they may not be hypovolemic.

Choice of fluid for resuscitation Three types of fluids frequently used today for active resuscitation are red blood cells, acellular colloid fluids with large mole-

secondary to a slightly higher sodium content administered as compared to what exists in our plasma (154 mEq verses 140 mEq) and 100 mL is actually pulled away from the intracellular compartment to be added to the interstitium. Crystalloids mainly expand the interstitial space, not the intravascular space, yet are used initially to

Regardless of mortality, different clinical scenarios may warrant the use of colloid versus crystalloid. cules that keep fluid intravascularly (hetastarch, dextran 40, albumin), and crystalloid fluids with added electrolytes (NaCl (0.9%), LR, Normosol). (See Fluid types and compositions.) Depending on the composition of certain fluids, varied amounts of fluid remain in the intravascular space for a certain length of time. For example, because more sodium exists in the extracellular compartment (intravascular and interstitial), fluids higher in sodium such as NaCl and LR will preferentially enter the interstitial space as sodium floats freely between the interstitium and blood vessels and water follows. Therefore, only 25% of a liter of NaCl will remain in the intravascular space. The 1,100 mL that actually enters into the extracellular fluid space is due to water shifts

18

resuscitate a patient with hypovolemia.

Colloid vs. crystalloid Both crystalloid and colloid solutions are considered effective for the resuscitation of a hypovolemic patient, as neither fluid provides a survival benefit that is superior to the other.14-16 Experts have conducted large studies on patients using colloids versus crystalloids in fluid resuscitation. Nineteen trials consisting of 1,315 participants (trauma, burns, and surgical patients) were done to compare differences in mortality between colloid and crystalloid resuscitation. The overall mortality difference was low (4%), or four deaths for every 100 patients resuscitated. The greatest difference noted between the use of colloids and crystalloids in that

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study was cost.17 A large trial known as the SAFE (Saline versus Albumin Fluid Evaluation) study was conducted between the years of 2001 and 2003, including mainly trauma and septic patients. Again, there was no difference found in 28 day outcomes which was defined as the number of days spent in the ICU, hospital length of stay, duration of mechanical ventilation, and duration of renalreplacement therapy.16 Regardless of mortality, different clinical scenarios may warrant the use of colloid versus crystalloid. For example, dehydrated patients secondary to vomiting, diarrhea, or diabetic ketoacidosis may require crystalloids first if there is no obvious blood loss. Another patient, who is malnourished and has chronic liver disease, may benefit from a colloid such as albumin, as they have low stores of this protein which normally helps keep fluid the intravascular space. Patients with poor cardiac function can benefit not only from blood products if they are ischemic, but also from crystalloids in order to promote flow and enhance cardiac output if volume is indicated. When trying to augment cardiac output and blood pressure, colloids have an advantage over crystalloid solutions, as a larger percentage enters the intravascular space and remains there for a longer period of time.2 This is because colloids provide the greatest effect on intravascular volume expansion and improve flow secondary to their low viscosity, which is equal to that of water.2 For example, up to 80% of a dextran 40 colloid www.nursing2008criticalcare.com

Advantages and disadvantages Price (per liter)

Fluid

Advantages

Disadvantages

Normal saline

• Interstitial fluid replacement • Not viscous

• Hyperchloremic metabolic acidosis • Large volumes lower pH • 25% in intravascular space

$1.46

Lactated ringers

• Interstitial fluid replacement • Buffer, maintains stable pH • Not viscous

• Not to be given with blood transfusions—calcium in LR would inhibit anticoagulant effect of citrate in PRBCs • 25% in intravascular space

$1.48

Albumin (5% and 25%) **Give with furosemide (Lasix) for optimal diuresis

• 70% intravascular fluid replace- • 25% albumin not good for initial resuscitation—small ment volumes administered • Rare reactions • Expensive • Volume expander • Buffer, antioxidant properties, inhibits platelet aggregation • Not viscous • Optimal for third spacing (pulmonary or peripheral edema), severe hypoalbuminemia/ malnutrition/cirrhosis/ARF

Hetastarch 6% **Limit use to 1,500 mL in 24 hrs

• Effective volume expander • Not viscous

• Inhibits Factor VII and von Willebrand Factor (vWF), impairs platelet adhesiveness, coagulation effects are dose dependent (> 1,500 mL/24 hrs)

Dextran **Limit use to < 20 mL/kg

• • • •

• Dose-related bleeding tendency, $14.96 impairs platelet aggregation, decreases levels of Factor VIII and vWF, enhances fibrinolysis

Hypertonic saline (3%, 7.5%)

• Possible benefit in head trauma • Cell dehydration (currently in use) • Less volume —expands intravascular volume with fluid shifts to decrease cerebral edema

Effective volume expander Dextran 70 lasts 12 hours Dextran 40 lasts 6 hours Not viscous

$30.63

$27.63

$5.00 or $13.00 per 500 mL, depends on brand)

(Griffel & Kaufman 1992, Imm & Carlson 1993, Jacob et al. 2005, Vincent et al. 2004, Chiara et al. 2003, Cooper et al. 2004)

solution enters and remains in the intravascular space. Three to 4 liters of crystalloid fluid would have to be given in order to equal the amount of 1 liter of colloid that remains in the intravascular space. Both crystalloids (NaCl, LR) and colloids (hetastarch, albumin 5%, 10% dextran 40) have equal viscosities and provide equal flow, www.nursing2008criticalcare.com

which in turn augments cardiac output and blood pressure.2

Possible complications Fluid resuscitation, as well as blood transfusions, can be beneficial to a hypovolemic patient, but risks and complications must always be taken into consideration with any treatment given. However, in the acute

phase of hypovolemia or shock, circulation is a priority and side effects from excess fluid are to be expected if the clinical status of a patient worsens. Adverse effects commonly seen in critically ill patients that may require immediate treatment are cerebral edema (which may lead to increased intracranial pressure), acute lung injury, acute

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Fluid balance and resuscitation

respiratory distress syndrome, transfusion related lung injury, abdominal compartment syndrome, and third spacing or edema.3 Large volumes may also dilute clotting factors and enhance bleeding (secondary coagulopathy), disrupt thrombus formation, and induce hypothermia. (See Advantages and disadvantages.)

volume resuscitation, which further exacerbates third spacing or peripheral edema. Critically ill patients with large amounts of edema are at risk secondary to many compounding factors in addition to their reason for being in the ICU. For example, hypoalbuminemic patients retain excess fluid and are prone to infection,

Hypoalbuminemic patients retain excess fluid and are prone to infection.

Third spacing Third spacing is usually apparent within the first few hours to days and can take weeks to resolve depending on the patient’s clinical course. As mentioned before, close to 70% of crystalloid infusions enter the interstitial space and don’t stay within the vasculature. There’s an associated hypoalbuminemia secondary to dilution from large

as edematous tissues easily break down into pressure ulcers secondary to poor circulation to the dependent areas of the body (scalp, back, sacrum, heels). It’s also common to see third spacing in sepsis, as well as septic and anaphylactic shock secondary to the capillary leak phenomenon, which is caused by cytokine activation and endothelial destruction. The presence of

third space edema, in conjunction with a positive fluid balance seen in hypotensive patients with acute renal failure, clearly indicates that the clinical appearance of patients doesn’t always match their hemodynamic status. Treatment of third spacing is effectively done with a colloid that has an oncotic pressure greater than or equal to the normal plasma oncotic pressure of 25 mm Hg.2 As shown in Choosing the right fluid, 25% albumin delivers the highest colloid oncotic pressure; however, it does not adequately replace volume for dehydrated or hypovolemic patients because it is administered in amounts of 50 to 100 mL. It therefore isn’t an initial choice in the acute phases of fluid resuscitation. However, it’s useful in relatively hypovolemic patients who are very edematous, as it assists in shifting excess fluid from the interstitial compartment back into the intravascular space.

Inside the ICU A fluid balance is not always able to be precisely calculated, which is why the patient’s clinical exam and hemodynamic status evaluated together may be a more accurate reflection of their

Choosing the right fluid Oncotic pressure (mm Hg)

Change in plasma volume

Duration of effect in intravascular space

10% dextran 40

40

1.5

6 hours

6% hetastarch

30

1.0 to 1.3

10 hours

5% albumin

20

0.1 to 1.3

16 hours

25% albumin

70

4.0 to 5.0

16 hours

Colloid fluid (infusion of 1 liter each)

(Halliwell 1988, Gan 1999, Moore 1965, Shires 1964, & Weil 2004)

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volume status. Vital signs are not as reliable as end points of resuscitation alone, as they lack detection of ischemia at the cellular level. Endpoints indicating ongoing tissue hypoperfusion include lactate, base deficit, and gastric mucosal pH. If abnormal, effective circulation must be restored and maintained to achieve homeostasis and end organ perfusion. Whether resuscitating with a crystalloid, colloid, or blood products, it’s important to accomplish stability rapidly. Further delays in fluid resuscitation in the face of impeding organ failure can only compromise a patient’s outcome and chance for an optimal recovery. ❖ REFERENCES 1. Poeze M, Solberg B, Greve JW, Ramsay G. Monitoring global volume-related hemodynamic or regional variables after initial

resuscitation: what is a better predictor of outcome in critically ill septic patients? Crit Care Med. 2005;33,2494-2500. 2. The ICU Book. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 2007. 3. Moore FA, McKinley BA, et al. Guidelines for shock resuscitation. J Trauma. 2006;61:82-89. 4. Friis-Hansen, B. Body water compartments in children: changes during growth and related changes in body composition. Pediatrics. 1961;28,169. 5. Maffly RH. The potential water in mammalian tissues. J Gen Physiology. 1959;42:1257. 6. Blowers AL, Irving M. Enterocutaneous fistulas. Surgery. 1992;10(2):27-31. 7. McIntyre PB. Management of enterocutaneous fistulas: a review of 132 cases. British J Surgery. 1984;71:293-296. 8. McGee S. Is this patient hypovolemic? JAMA. 1999;281:1022-1029. 9. Committee on Trauma. Advanced Trauma Life Support Student Manual. Chicago, Ill: American College of Surgeons. 2004:47-59. 10. Scalea TM, Maltz S, Yelon J, et al. Resuscitation of multiple trauma and head injury: role of crystalloid fluids and inotropes. Crit Care Med. 1994;20:1610-1615. 11. Abou-Khalil B, Scalea TM, Trooskin SZ, et al. Hemodynamic responses to shock in young trauma patients. Crit Care Med. 1994;22,633-639. 12. Huckabee WE. Abnormal resting blood

lactate. The significance of hyperlactatemia in hospitalized patients. Am J Med. 1961;30:833. 13. Porter JM, Ivatury RR. In search of the optimal end points of resuscitation in trauma patients: a review. J Trauma. 1998; 44:908-914. 14. Choi PT-L, Yip G, Quinonez LG, et al. Crystalloids vs. colloids in fluid resuscitation: a systematic review. Crit Care Med. 1999;27:200-210. 15. Wilkes MN, Navickis RJ. Patient survival after human albumin administration: a meta-analysis of randomized, controlled trials. Ann Int Med. 2001;135:149-164. 16. The Safe Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. New Eng J Med. 2004;350:2247-2256. 17. Schierhout G, Roberts I. Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: a systematic review of randomized trials. British Med J. 1998; 316:961-964. Wendy J. Stevens is in the Dept of Critical Care, Surgery, and Trauma, St. Luke’s Hospital, Bethlehem, Pa. The author has disclosed that she has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity. Adapted from: Stevens WJ. Fluid balance and resuscitation: critical aspects of ICU care. Men in Nursing. 2007;2(6):16-23.

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Fluid balance and resuscitation: Critical aspects of ICU care GENERAL PURPOSE: To provide the registered professional nurse with current information about fluid balance and resuscitation. LEARNING OBJECTIVES: After reading the preceding article and taking the following test, the nurse should be able to: 1. Describe the physiology of the fluid compartments and their status in fluid imbalances. 2. Identify signs and symptoms of fluid imbalance and appropriate assessment parameters. 3. Discuss treatment modalities used for fluid resuscitation.

1. Which of the following is a true statement about fluid distribution and resuscitation? a. The type of fluid used determines the time fluid resuscitation should start. b. Water is present in higher quantities in people who have more fat. c. The percentage of fluid in each body compartment is inconsistent for every adult. d. A patient may be in shock despite having a normal blood pressure and heart rate.

c. its primary role is in the intracellular compartment. d. it crosses the capillary membrane too freely. 6. An example of relative hypovolemia is patient who a. is hemorrhaging. b. has an open abdomen. c. has a high output fistula. d. has diarrhea.

11. In addition to sodium and lactate, which laboratory values are important indicators of volume status? a. potassium and blood urea nitrogen b. urine specific gravity c. urobilinogen and uric acid d. creatinine and hemoglobin

2. Which signs and symptoms are typically seen in the early stages of hypovolemia? a. slow capillary refill, unequal pupils, and dizziness b. weak peripheral pulses, cyanosis, and petechiae c. tachycardia, lethargy, and anxiety d. shortness of breath, lack of tears, and weight loss

7. An example of absolute hypovolemia is a patient who has a. septic shock. b. copious pulmonary secretions. c. third space fluid in the interstitial compartment. d. high output fistulas.

12. Which of the following signs are associated with low magnesium levels? a. slurred speech, metabolic acidosis, and seizures b. polydipsia, dehydration, and hypotension c. excessive thirst, coma, and confusion d. weakness, vomiting, and depressed T waves

3. Because of their percentage of total body water, which patient would be at greatest risk from a substantial fluid loss? a. a 6-month-old infant b. a 17-year-old adolescent c. a lean adult d. an obese adult

8. Despite normal urine output (UOP) and vital signs, tissue hypoperfusion at the cellular level may be indicated by all of the following except a. serum sodium less than 135 mEq/L. b. lactate levels greater than 4. c. base deficit greater than -4. d. mixed venous oxygen saturation less than 60%.

13. One disadvantage of using lactated ringers in fluid resuscitation is that a. it can produce hyperchloremic metabolic acidosis. b. large volumes lower pH. c. it should not be given with blood transfusions. d. it impairs platelet adhesiveness and coagulation.

4. The osmolality of the extracellular and intracellular fluid compartments is determined by the concentration of a. potassium in the extracellular compartment. b. albumin in the extracellular compartment. c. sodium in the extracellular compartment. d. sodium in the intracellular compartment.

9. Which indicator is linked to a higher mortality rate if not corrected quickly in hemodynamically unstable patients? a. elevated lactate b. increased base deficit c. mixed venous oxygen saturations d. low UOP

14. Which is used initially to resuscitate a patient with hypovolemia? a. crystalloid solutions c. blood b. colloid solutions d. fresh frozen plasma

5. Albumin is often not a first choice for fluid resuscitation because a. of cost and availability issues. b. it does not allow adequate maintenance of colloidal pressure.

10. Despite normal serum lactate and base deficit levels, organ tissue oxygen deficits may be evidenced by a. heart rate. b. UOP.

c. gastric pH. d. blood pressure readings.

15. How much whole blood does a 70 kg female have? a. 5.3 liters c. 2.5 liters b. 4.2 liters d. 1.6 liters 16. Which fluid is used for treating third spacing? a. normal saline c. dextran b. hetastarch 6% d. albumin

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Last name ____________________________ First name ________________________ MI _____ Address _______________________________________________________________________________ City _______________________________________ State _________________ ZIP ______________

Job title _______________________________ Specialty _________________________________ Type of facility _______________________________ Are you certified? ❑ Yes ❑ No Certified by _________________________________________________________________________ State of license (1) __________________________ License # _________________________

State of license (2) __________________________ License # _________________________ Telephone ___________________ Fax ___________________ E-mail ______________________ ❑ Please fax my certificate to me. Registration Deadline: April 30, 2010 ❑ From time to time, we make our mailing list available to outside organizations to announce special offers. Please check here if you do not wish us to release your name and address. Contact hours: 2.5 Pharmacology hours: 0.0 Fee: $24.95 B. Test Answers: Darken one circle for your answer to each question.

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C. Course Evaluation* 1. Did this CE activity's learning objectives relate to its general purpose? ❑ Yes ❑ No 2. Was the journal home study format an effective way to present the material? ❑ Yes ❑ No 3. Was the content relevant to your nursing practice? ❑ Yes ❑ No 4. How long did it take you to complete this CE activity?___ hours___minutes 5. Suggestion for future topics _________________________________________________________

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D. Two Easy Ways to Pay: ❑ Check or money order enclosed (Payable to Lippincott Williams & Wilkins) ❑ Charge my ❑ Mastercard ❑ Visa ❑ American Express Card # ____________________________________________ Exp. date __________________ Signature _____________________________________________________________________

*In accordance with the Iowa Board of Nursing administrative rules governing grievances, a copy of your evaluation of the CE offering may be submitted directly to the Iowa Board of Nursing. CCN0308