Pressure Ulcers: What Clinicians Need to Know
William T Wake, MD, FAAFP
Summer 2010 - Volume 14 Number 2
Pressure ulcer treatment is one of many aspects of patient care in which nursing care interfaces directly with clinician-provided medical services. Traditionally, the treatment of pressure ulcers has been left to nurses. No less an authority than Florence Nightingale said in 1859, “If he has a bedsore, it’s generally not the fault of the disease, but of the nursing.”1
Physicians have tended to be passive participants, routinely cosigning orders written by hospital-based wound-care nurses or home health nurses. Realization of the costs associated with the treatment of pressure ulcers and recent requirements by third-party payers have prompted physicians to become more actively engaged in the prevention, identification, and treatment of pressure ulcers.
Pressure ulcers are localized areas of tissue damage or necrosis that develop because of pressure over a bony prominence. They have previously been called pressure sores, bedsores, and decubitus ulcers, terms that imply that only bed-bound, nonambulatory patients develop pressure ulcers. It is important to recognize that patients who are ambulatory can also develop pressure ulcers, although reduced mobility is still a major risk factor.
The purpose of this article is to familiarize physicians and other clinicians who provide care to hospitalized patients, such as physician assistants, certified nurse midwives, and nurse practitioners, with some of the terminology associated with pressure ulcers, so that they can better assess patients at risk for the development of pressure ulcers and properly identify and describe pressure ulcers.
For a sense of the total costs of the treatment of pressure ulcers, data from the 1990s, although old, can shed a light on current costs. In 1996, $6.4 billion was spent on pressure ulcers, which was 1.2% of total health care costs in the US.2 In 2006, excluding neonatal and maternal conditions, almost $11 billion was paid out for hospital stays in which pressure ulcer was either a primary or secondary diagnosis.3 For the individual patient, the current costs of providing care for one pressure ulcer can range from $3500 to over $60,000, depending on the stage of the ulcer.4
Pressure ulcers have also attracted the attention of the medicolegal community. Some courts regard pressure ulcers as evidence of elder abuse, and some lawsuits have awarded judgments of more than $10 million.5 If the presence of pressure ulcers is considered to indicate elder abuse, such legal judgments are not covered by conventional medical malpractice insurance policies, nor are such awards limited by the caps imposed by many US states in medical malpractice lawsuits.
In November 2008, the Center for Medicare and Medicaid Services instituted a policy to withhold reimbursement due to be made to acute-care hospitals for the costs of treating hospital-acquired conditions,6 such as pressure ulcers. Although hospitals will be paid for the care of pressure ulcers that originated before admission, hospital-acquired pressure ulcers would be the responsibility of the admitting hospital. Because of this change in policy, there is now an incentive for hospitals to accurately assess for skin problems in all patients being admitted and to identify all patients at risk for developing pressure ulcers so that preventive measures can be put in place. Increasingly physicians are being called on to identify at-risk patients and accurately classify skin conditions present at admission.
Identification and Risk Assessment
On admission to an acute-care hospital, all patients should undergo a thorough skin assessment to determine if they are being admitted with skin conditions, including pressure ulcers, that were already present. Any such condition must be clearly documented on the record of the admission physical examination. This documentation is ultimately the responsibility of the admitting physician.
In addition to performing a complete skin assessment, it is also important to identify the patient who may be at risk for developing a pressure ulcer after admission to the hospital. Such identification should then initiate interventions intended to maintain skin integrity and prevent skin breakdown. The most common assessment tool used for this purpose is the Braden scale,7,8 which evaluates the severity of several different factors that would place the patient at risk for the development of a pressure ulcer:
- Sensory: how well a patient can process sensory input from the skin as well as how effectively s/he can communicate level of sensation
- Moisture: to what degree the skin is exposed to moisture
- Activity: how active a patient is, irrespective of his or her degree of mobility
- Mobility: how well the patient can change and control his or her body position
- Nutrition: what constitutes the usual pattern and amount of caloric intake
- Friction and shear: how the patient moves within his or her confines.
Each of these factors is ranked on a numeric scale from 1 to 4, with the exception of friction and shear, which only has three points on its scale. Scores are then totaled. Ultimate risk is determined by the total Braden score, with the highest possible score being 23. Patients with scores of 18 or less are considered to be at varying degrees of risk. Individual hospitals will establish their own criteria for the specific levels of risk associated with the range of Braden score.
The performance of an assessment using the Braden scale is within the scope of practice of all registered nurses who have been educated to use the tool. Braden-scale assessments should be done on a regular basis, with the frequency determined by individual hospital policy, for all confined patients, as well as for patients who experience any change of condition, who have been transferred between different hospital units, or who have just returned from surgery. A physician should be able to ask for and to receive an up-to-date Braden score for any patient admitted to the hospital. The frequency of Braden-scale assessments should be at least every three days. Interventions can then be based on the specific deficiency identified by the assessment.
Patients who have problems with mobility will have to be physically turned by hospital staff on a regular basis. Repositioning frequency will be determined by the individual’s tissue tolerance, level of activity and mobility, general medical condition, the overall treatment objectives for the patient, and assessments of the individual’s skin condition.9 Patients with excess skin moisture will have to be treated with drying agents and compounds intended to protect exposed areas from maceration. Friction and shear can result in the disruption of capillaries and other small vessels, producing ischemia in subcutaneous tissues. When patients must move in bed, they must be lifted and repositioned, not slid across the mattress.
Nutritional deficits are common in many hospital-based patient populations and deserve special consideration. Protein supplementation is important, but there should be ongoing assessment with review of albumin and prealbumin levels. It can be useful to identify a patient at risk for nutritional deficiency by checking the initial serum albumin level. However, to assess for effectiveness of nutritional intervention, a prealbumin level, with a half-life of two days, is far more useful and will change during a period of days to one week with effective nutritional support.10
Using the Braden scale allows for a systematic approach to risk assessment and provides a road map that clinicians can use to efficiently manage the interventions intended to prevent the development of pressure ulcers.
When ulcers are identified in a hospitalized patient, it is essential to carefully document the circumstances that led to the formation of the ulcer, where the ulcer is, how large it is, and what stage it is. Different interventions and types of reimbursed procedures are required, depending on the stage of the ulcer. Only pressure ulcers can be staged. Ulcers that may have other causes, such as venous insufficiency, arterial occlusive disease, and diabetes mellitus, are not appropriate for the type of staging that is described here.
The stage of a pressure ulcer depends on the depth of the ulcer. Figure 1 shows the various stages of pressure ulcers by layer of skin or subcutaneous tissue involvement.11 The total surface area that the ulcer encompasses is not the determining factor. For example, a stage I or II pressure ulcer may have a fairly large surface area, but a stage III or IV may be of relatively smaller diameter but of greater depth. The development of pressure ulcers is a progressive process. If a patient has a lower-stage pressure ulcer and if preventive measures are not implemented to address the factors contributing to its development, then it will progress into a more complicated and severe ulcer.
In stage I ulcers, there is a change in the color, consistency, or temperature of the skin, but the skin is intact and the underlying tissues are unaffected. Figure 2 demonstrates a typical appearance; however, in some cases the skin may appear normal, and it is only by tactile examination that any changes in skin integrity can be identified. A stage I pressure ulcer is a warning sign that there is a problem. Interventions at this point can help prevent further, more problematic skin conditions.
Stage II pressure ulcers involve the epidermal layer of skin and may extend into the dermis as well. These usually appear as shallow, open areas or intact serum-filled or serosanguineous blisters. Although the skin is physically intact in a stage I pressure ulcer, a stage II pressure ulcer involves a break in the skin’s integrity. Figure 3 depicts a typical example of a stage II pressure ulcer, with excoriation of the involved skin and extension into deeper tissues. When a patient develops a stage II pressure ulcer, it is common to have to contend with issues such as serous drainage that complicate skin care and can cause problems with adjacent areas of the skin that would not otherwise be affected.
Stage III pressure ulcers, such as the one seen in Figure 4, extend into the subcutaneous tissue, and although underlying bone, muscle, and fascia may be visible, the ulcer has no direct involvement of these structures. The presence of any necrotic slough in an ulcer that otherwise appears to be a stage II pressure ulcer automatically qualifies that ulcer to be a stage III ulcer. Stage III pressure ulcers may also involve tunneling and undermining, wherein the ulcer extends beneath normal tissue.
Stage IV pressure ulcers extend into bone or muscle, as is seen in Figure 5. Patients outside of acute-care hospitals with stage III and stage IV pressure ulcers qualify for Medicare Durable Medical Equipment coverage for more specialized mattresses and hospital beds.
Because staging is based on the depth of involvement, it is essential to be able to visualize the bottom of the ulcer. If the bottom of the ulcer is covered by thick eschar or adherent slough, then it cannot be staged and is referred to as unstageable. Only when the eschar is débrided and the base of the ulcer is fully visualized can the ulcer be accurately staged. An example of this is shown in Figure 6.
Another type of pressure ulcer that is difficult to stage is designated a deep tissue injury. The surface of the skin may appear to be like that of a stage I or II ulcer, as is shown in Figure 7,12 but the damage to underlying tissues is severe. Because the pressure forces are greatest at the interface between bone and surrounding soft tissue, tissues not visible may be severely compromised, even necrotic. Figure 8 shows how severe and how deep the damage can be to deep tissues.13 Areas of the skin with deep tissue injury can rapidly progress into deep stage III or IV ulcers, appearing to seemingly materialize overnight. The clinician’s index of suspicion regarding these ulcers must be high. A patient with what appears to be a large stage I or II pressure ulcer who also has a low Braden score may very well have deep tissue injury. In Europe, deep tissue injury and unstageable pressure ulcers are classified as stage IV.9 Whatever classification is used, these patients should be treated as if they have a stage III or IV pressure ulcer.
Although it is only too easy to fall into the paradigm of watching pressure ulcers progress from stage I to stages III or IV, treatment must be rendered with the expectation of the ulcer healing from a stage III or IV to stage I and hopefully even back to more normal skin and tissue integrity.
The major principles of pressure ulcer treatment are as follows:
- Eliminating external pressure on affected area(s) of the body
- Preserving the integrity of surrounding normal skin and tissues
- Facilitating the body’s own mechanisms of natural healing
- Removing necrotic and devitalized tissue
- Providing adequate pain relief
- Reducing bacterial load
- Treating conditions that place the patient at risk for developing pressure ulcers, such as malnutrition and anemia.
It is beyond the scope of this article to review in detail the spectrum of treatment modalities available to treat pressure ulcers. The European Pressure Ulcer Advisory Panel and National Pressure Ulcer Advisory Panel have recently published a joint report on guidelines for treatment of pressure ulcers.9 Recommendations related to each of these principles are provided in that report, which can be accessed at www.npuap.org.
A 2008 review of treatment options that comprehensively surveyed the medical literature for all studies related to the treatment of pressure ulcers concluded, “Clinicians should make decisions regarding pressure ulcer therapy based on fundamental wound care principles, cost, ease of use, and patient preference.”14 A more practical recommendation for clinicians is to consult the certified wound-care specialists at the particular medical center in which they practice regarding what is available and what would be best to offer their patients with pressure ulcers.
Whether they were called bed sores or decubitus or some other even more archaic terms, pressure ulcers have been part of the spectrum of medical and nursing care since even before Florence Nightingale attended to the wounded soldiers of the Crimean War. For most of that time, our nursing colleagues might have thought that they had to contend by themselves with treating these conditions. It can be hoped that more involvement by physicians with the treatment of pressure ulcers will increase scientific study of the pathophysiology of pressure ulcers and effective treatment options. With such knowledge, it is possible that recommendations based on evidence can be made so that efficacy will improve and cost will decrease. Partnerships between physicians and nurses can help solve clinical problems by bringing fresh perspectives to the analysis process. The ultimate beneficiaries will be our patients, who depend on the collaboration of physicians and nurses to successfully address their personal health care needs.
The author(s) have no conflicts of interest to disclose.
Katharine O’Moore-Klopf, ELS, of KOK Edit provided editorial assistance.
1. Nightingale, Florence. Notes on nursing: what it is, and what it is not. New York: D Appleton and Company; 1860.
2. Pompeo MQ. The role of “wound burden” in determining the costs associated with wound care. Ostomy Wound Manage 2001 Mar;47(3):65–71.
3. Russo CA, Steiner C, Spector W. Statistical Brief #64: Hospitalizations related to pressure ulcers among adults 18 years and older, 2006 [monograph on the Internet]. Rockville, MD: US Agency for Healthcare Research and Quality: Healthcare Cost and Utilization Project (HCUP); 2008 Dec [cited 2010 Apr 5]. Available from: www.hcup-us.ahrq.gov/reports/statbriefs/sb64.jsp.
4. Pressure ulcers [monograph on the Internet]. Publication 1999/23. The Hague: Health Council of the Netherlands; 1999 Dec 31 [cited 2010 Apr 5]. Available from: www.gezondheidsraad.nl/en/publications/pressure-ulcers.
5. Voss AC, Bender SA, Ferguson ML, Sauer AC, Bennett RG, Hahn PW. Long-term care liability for pressure ulcers. J Am Geriatr Soc 2005 Sep;53(9):1587–92.
6. Centers for Medicare and Medicaid Services (CMS), HHS. Medicare program; changes to the hospital inpatient prospective payment systems and fiscal year 2008 rates. Fed Regist 2007 Aug 22;72(162):47129-8175.
7. Braden B, Bergstrom N. A conceptual schema for the study of the etiology of pressure sores. Rehabil Nurs 1987 Jan-Feb;12(1):8-12.
8. Bergstrom N, Braden BJ, Laguzza A, Holman V. The Braden Scale for Predicting Pressure Sore Risk. Nurs Res 1987 Jul-Aug;36(4):205–10.
9. European Pressure Ulcer Advisory Panel and National Pressure Ulcer Advisory Panel. Prevention and treatment of pressure ulcers: quick reference guide [monograph on the Internet]. Washington DC: National Pressure Ulcer Advisory Panel; 2009 [cited 2010 Apr 5]. Available from: www.epuap.org/guidelines/Final_Quick_Prevention.pdf.
10. Shenkin A. Serum prealbumin: is it a marker of nutritional status or of risk of malnutrition? Clin Chem 2006 Dec;52(12):2177–9.
11. Auerbach PS. Wilderness medicine. 5th ed. St Louis, MO: Mosby; 2007.
12. Black JM, Black SB. Unusual wounds: deep tissue injury. Wounds 2003 Nov 10;15(11):38.
13. Pressure ulcer staging illustrations [monograph on the Internet]. Washington, DC: National Pressure Ulcer Advisory Panel; 2007 [cited 2010 Apr 24]. Available from: www.npuap.org/resources.htm.
14. Reddy M, Gill SS, Kalkar SR, Wu W, Anderson PJ, Rochon PA. Treatment of pressure ulcers: a systematic review. JAMA 2008 Dec 10;300(22):2647–62.
More from this Journal section
Image Diagnosis: Ankle Fractures and Dislocations
Friday, 11 June 2010
Sundeep R Bhat, MD; Gus M Garmel, MD, FACEP, FAAEM Summer 2010 - Volume 14 Number 2 Figure 1. Anterior-posterior view of the ankle Standard radiographs for suspected ankle injury include anteriorposterior (AP), lateral, and mortise views.1,2 On this AP radiograph, the solid white arrow demonstrates a subtle fracture of the distal fibula; the ankle mortise is intact. On AP ankle films, cortical disruption or talar tilt should be identified. If tibiofibular overlap (TFO)—the distance between the lateral border of the tibia and the medial border of the fibula—is less than 10 mm, or the tibiofibular clear space (TCS)—the distance between the medial border of the fibula and the lateral aspect of the posterior tibial malleolus—is greater than 5 mm, associated syndesmotic injury is likely. Greater than 2 mm difference between the lateral and medial joint space above the talus indicates talar tilt suggestive of medial or lateral disruption of this joint.1,2 Figure 2. Bimalleolar Ankle Fracture Anterior-posterior (AP) view (left) of the ankle demonstrates fracture of the fibula visualized as cortical disruption along the lateral border and a subtle distal tibia fracture seen approximately 2 mm above the distal tip, with preservation of the posterior border of the tibia (seen on lateral view [right]). In addition, the AP view reveals widening of the medial aspect of the superior talar joint space compared with the lateral space, suggesting talar tilt. This pattern of distal fibula fracture with medial malleolus involvement is often due to supination-external rotation injury and is likely associated with significant joint instability if the deltoid ligament is disrupted.1 A small avulsion of the talar neck is also seen along the medial border, opposite the site of the distal tibia fracture. Figure 3. Trimalleolar Ankle Fracture Anterior-posterior (AP) (left) and lateral (right) views demonstrate fracture of the distal fibula, medial malleolus, and posterior tibial malleolus with associated shortening. Note the decreased tibiofibular overlap (TFO) and significant talar tilt on the AP radiograph. Fractures that can’t be reduced or which involve widening of the ankle mortise require urgent
orthopedic consultation for possible open reduction internal fixation (ORIF) to prevent complications of avascular necrosis, malunion, or nonunion. Subtle nondisplaced fractures or displaced ankle fractures that have been anatomically reduced can be treated with a posterior splint and stirrup, crutches and nonweight-bearing, with close orthopedic follow-up.1 Figure 4. Talar neck fracture-dislocation Slightly oblique anterior-posterior radiographs show a talar neck fracture-dislocation with associated subluxation of the subtalar joint pre- and postreduction. The talus was reduced into better anatomic position, but talar tilt and joint instability are still evident postreduction. Open ankle fractures (such as this case) are surgical (orthopedic) emergencies, requiring immediate reduction, irrigation and antibiotics, and tetanus vaccination if indicated. This Hawkins Type IV fracture has a near 100% likelihood of avascular necrosis due to the extreme level of displacement.3 References 1. Ankle fractures. In: Koval KJ, Zuckerman JD. Handbook of fractures. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. p 398-423. 2. del Castillo J. Foot and ankle injuries. In: Adams JG. Emergency medicine. 1st ed. Philadelphia, PA: Saunders Elsevier; 2008. p 897-909. 3. Talus. In: Koval KJ, Zuckerman JD. Handbook of fractures. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. p 435-42.
ECG Diagnosis: Wolff-Parkinson-White Syndrome
Thursday, 27 May 2010
Joel T Levis, MD, FACEP, FAAEM Summer 2010 - Volume 14 Number 2 Wolff-Parkinson-White Syndrome (WPWS) is defined as the presence of an accessory pathway (AP) and has a predisposition to the development of supraventricular tachydysrhythmias. Conduction over an AP circumvents conduction delay occurring within the atrioventricular node (AVN), which leads to early eccentric activation of the ventricles and fusion complexes.1 If WPWS with atrial fibrillation (AF) is treated by drugs that prolong the AVN refractory period (eg, calcium-channel blockers, beta-blockers, digoxin, adenosine), the rate of conduction through the AP may increase and degenerate to ventricular fibrillation (VF).2 Unstable patients with WPWS and AF should receive immediate electrical cardioversion.3 Stable patients can be chemically cardioverted with IV procainamide. Amiodarone should be used with caution due to its ability to cause ventricular rate acceleration and degeneration into VF.3 Ibutilide is considered an alternative agent, although it has numerous side effects.1 Cardiology or electrophysiology consultation with consideration for radiofrequency mapping and ablation should occur for patients presenting with AF in the setting of WPWS. References 1. Levis JT, Garmel GM. Atrial fibrillation with Wolff-Parkinson-White syndrome. Internet J Emerg Med [serial on the Internet] 2009 [cited 2010 Mar 8];5(1) [about 1 p]. Available from: www.ispub.com/ostia/index.php?xmlPrinter=true&xmlFilePath=journals/ijem/vol5n1/wpw.xml. 2. Garmel GM. Wide complex tachycardias: understanding this complex condition: Part 1—epidemiology and electrophysiology. West J Emerg Med 2008 Jan;9(1):28-39. 3. Fengler BT, Brady WJ, Plautz CU. Atrial fibrillation in the Wolff-Parkinson-White syndrome: ECG recognition and treatment in the ED. Am J Emerg Med 2007 Jun;25(5):576-83.
Image Diagnosis: Abnormal Plain Films from the Emergency Department
Friday, 02 July 2010
Gus M Garmel, MD, FACEP, FAAEM Summer 2009 - Volume 13 Number 3 Case 1. Soft tissue lateral neck x-ray demonstrating acute epiglottitis. The epiglottis is swollen and looks like a thumbprint (thumbprint sign) at the level of the hyoid bone. A normal epiglottis in a true soft tissue lateral neck is thin. The epiglottis can be directly visualized using nasopharyngoscopy or direct laryngoscopy in skilled hands. Because of the Haemophilus influenzae type b (HIB) vaccine and herd immunity, this condition is relatively rare in children. It may still occur in adults, although it tends to result in less airway compromise because the adult airway has a larger diameter. Despite this, epiglottitis remains an airway emergency, requiring close observation and potential emergent airway intervention. Case 2. Plain abdominal film (erect) demonstrating free air under both hemidiaphragms. A small sliver of free air (black) is seen on close inspection directly under the diaphragms in this upright film. In the appropriate clinical setting, a patient with abdominal pain and free air on plain film is an ominous sign. Free air may be present in postoperative patients and has been reported following vigorous sexual activities.
Hyponatremia—What Is Cerebral Salt Wasting?
Tuesday, 08 June 2010
Corridor Consult Jasminder Momi, MD; Christopher M Tang, MD; Antoine C Abcar, MD; Dean A Kujubu, MD; John J Sim, MD Summer 2010 - Volume 14 Number 2 Abstract Background: Hyponatremia is a common electrolyte imbalance in hospitalized patients. It is associated with significant morbidity and mortality, especially if the underlying cause is incorrectly diagnosed and not treated appropriately. Often, the hospitalist is faced with a clinical dilemma when a patient presents with hyponatremia of an unclear etiology and with uncertain volume status. Syndrome of inappropriate antidiuretic hormone (SIADH) is frequently diagnosed in this clinical setting, but cerebral salt wasting (CSW) is an important diagnosis to consider. Objective: We wanted to describe the diagnosis, treatment, and history of CSW to provide clinicians with a better understanding of the differential diagnosis for hyponatremia. Conclusion: CSW is a process of extracellular volume depletion due to a tubular defect in sodium transport. Two postulated mechanisms for CSW are the excess secretion of natriuretic peptides and the loss of sympathetic stimulation to the kidney. Making the distinction between CSW and SIADH is important because the treatment for the two conditions is very different. Case Presentation A man, age 43 years, is evaluated for hyponatremia. He was admitted to the hospital six days earlier for an intracranial hemorrhage that required emergency evacuation. The patient was later extubated when his neurologic status improved. His medical history includes poorly controlled hypertension and rheumatoid arthritis. On hospital day 6, his serum sodium level is noted to be 121 mEq/L. He has been receiving 0.9% normal saline since admission, and his sodium level has been gradually decreasing from 141mEq/L, the level at admission. A hyponatremia workup reveals a low serum osmolarity of 256 mOsm/kg, a normal serum creatinine level of 0.6 mg/dL, a urine sodium level of 89 mmol/L, and an inappropriately high urine osmolarity of 588 mOsm/kg. His urinalysis reveals a specific gravity of 1.030, with no blood or protein. His levels of serum thyroid-stimulating hormone and random cortisol are within normal limits. His brain natriuretic peptide (BNP) and fractional excretion of uric acid are elevated, at 686 pg/mL and 83.8%, respectively. The patient appears euvolemic, with a blood pressure of 115/70 mm Hg and pulse of 90 beats per minute. His intake and outtake documentation reveals that his urine output has been 2 to 4 L/d despite a fluid restriction of <1.5 L/d that was initiated two days earlier. His sodium level has continued to decline after the fluid restriction. The working diagnosis is syndrome of inappropriate antidiuretic hormone (SIADH). Background Hyponatremia (sodium level of <136mEq/L) has been associated with confusion, lethargy, seizures, coma, and even death.1 The differential diagnosis for hyponatremia is broad and includes hormone disorders (eg, thyroid and adrenal insufficiency), medications, and volume-related problems. In the acute-care setting, hyponatremia has been reported to occur in up to 30% of patients with subarachnoid hemorrhage (SAH).2,3 The physician often faces a clinical dilemma when hyponatremia has an unclear etiology and volume status is uncertain. Early and accurate diagnosis of the etiology of the hyponatremia is important in order to institute proper therapy. An incorrect diagnosis can cause significant morbidity and mortality. SIADH is a frequent diagnosis in a patient with hyponatremia and a concurrent intracranial process.4 However, cerebral salt wasting (CSW) is an important diagnosis to consider and differentiate from SIADH. CSW was first described by Peters et al in 19505 when they reported the cases of three patients with an intracranial process who exhibited renal salt wasting, but the existence of CSW was questioned after the identification of SIADH in 1957 by Schwartz et al.6 For years afterward, CSW was considered either a condition that was an element of SIADH or one that did not exist. CSW now is again being recognized as a separate entity altogether. A retrospective review of data for 316 patients who presented with SAH and hyponatremia found that the diagnosis was SIADH in 69% and was CSW in 6.5%.7 Both conditions have been reported to occur in the setting of head trauma, intracranial or metastatic neoplasm, carcinomatous or infectious meningitis, SAH, and central nervous system surgery.8 The distinction between these two conditions is important because their treatments are different. Diagnosis CSW and SIADH share many similar laboratory and clinical findings (Table 1). Both conditions present with low serum osmolality, high urine osmolality, and a high urine sodium level. The fundamental difference between the two processes is the extracellular fluid volume (ECFV) status. CSW is defined by the renal loss of salt with concomitant extracellular fluid loss.2,3,8-10 Consequently, patients with CSW have hypovolemia compared with patients with SIADH, who have euvolemic or mild ECFV expansion. The clinical history and assessment findings may be helpful if postural blood pressure changes, tachycardia, or poor skin turgor are present. Unfortunately, this difference is not always clinically apparent. In a study conducted by Chung et a11 to evaluate the clinical assessment of the ECFV status in 58 patients without edema and hyponatremia, only 47% of those with hypovolemia and 48% of those with euvolemia were accurately classified. Uric acid excretion may be one measure for differentiating between CSW and SIADH. Initially, both conditions are associated with a low serum uric acid level and a high fractional excretion of uric acid.4,8,9 Uric acid is normally resorbed in the proximal tubule along with sodium. In SIADH, sodium resorption in the proximal tubule may be decreased because of an expanded ECFV, which can lead to less uric acid absorption and increased uric acid loss in the urine. Another contributing mechanism in SIADH, proposed by Decaux et al,12 involves the stimulation of the V1 receptor by antidiuretic hormone, which enhances excretion of uric acid in the renal tubules. The exact mechanism of uric acid loss in CSW has not been well defined. It is generally believed to be part of the solute diuresis that occurs in CSW with impaired urate transport in the proximal tubules.4,8 The key differentiation is that patients with SIADH have a serum uric acid level and fractional excretion of uric acid that normalize after correction of the serum sodium level, whereas the uric acid level remains low and uric acid excretion remains elevated in patients with CSW, despite correction of hyponatremia.2,4,8,9 Response to fluid therapy is also a key distinction between SIADH and CSW. The treatment of choice for SIADH is free water restriction when increased fluid intake will worsen the hyponatremia. In contrast, CSW is a volume-depleted and sodium-wasting state requiring fluid replacement with isotonic solutions. The renal wasting of sodium in CSW is poorly understood. Two postulated mechanisms are disruption of sympathetic neural input to the kidney and natriuresis induced by natriuretic peptides. Both mechanisms can lead to downstream inhibition of the renin-angiotensin-aldosterone system.2,4,8,9 Sympathetic stimulation normally causes proximal tubule absorption of sodium. Depression of this sympathetic input to the kidney results in less sodium resorption in the proximal tubule and an increase in sodium delivery to the distal tubule. This leads to a decrease in the effective arterial blood volume, triggering the baroreceptors to release antidiuretic hormone to help maintain intravascular volume. A depressed sympathetic drive has also been associated with a decrease in renin and aldosterone levels, further inhibiting sodium retention.2,4,8,9 Elevated natriuretic peptides levels have been described with CSW.13 Atrial natriuretic peptide (ANP) and BNP have both been studied in patients with intracranial pathology and hyponatremia. Although both ANP and BNP have been described to be elevated for up to two weeks, BNP elevation is more consistent. BNP is primarily released by the cardiac ventricles in response to the increased ECFV but can also be secreted by the brain.13 The natriuretic peptides have been described as causing direct tubular inhibition of sodium resorption and inhibition of intramedullary collecting-duct sodium absorption.8,9,13 They are also believed to cause direct inhibition of renin and aldosterone release from the juxtaglomerular cells and the adrenal gland, respectively.8,9,13 Berendes et al13 studied BNP levels in patients with an intracranial process and compared them with study control participants. Sixty patients were divided into three groups. Group 1 included 10 patients with SAH who underwent clipping of ruptured aneurysms within 24 hours, group 2 included 10 patients with intracranial tumors who underwent craniotomy, and group 3 included 40 healthy individuals. Natriuretic peptides (ANP, BNP), aldosterone, renin, and antidiuretic hormone levels were assessed before surgery and at 1 hour, 4 hours, 12 hours, and daily for 7 days after surgery. Patients with SAH had elevated baseline BNP levels but normal ANP levels when compared with healthy individuals. Urine output and urinary excretion of sodium were greater in the SAH group than in the other groups. Aldosterone levels were also lower in this group. BNP appeared to be the primary natriuretic peptide that caused salt wasting in patients with SAH. Treatment Early appropriate therapy of hyponatremia is important to prevent complications. CSW is a volume-depleted state treated with intravenous administration of isotonic or hypertonic fluids to obtain positive fluid balance and correct volume depletion. Depending on the acuity and clinical manifestation of the hyponatremia, isotonic or hypertonic solutions would be indicated. Additionally, sodium tablets can be combined with the intravenous fluids. Doses of sodium of up to 12 g/d may be used.2 Rapid correction of the serum sodium by more than 12 mmol/d should be avoided because of the risk of osmotic demyelination.1 Once euvolemia is achieved, the goal of therapy is to maintain a positive salt balance and to prevent volume depletion by matching the urinary output with volume repletion. Fludrocortisone, a potent mineralocorticoid, has also been used for the treatment of CSW at doses of 0.1 to 1 mg/d. It exerts its effects by stimulating reabsorption of sodium and water in the distal tubule, leading to expansion of the ECFV. When fludrocortisone therapy was used in patients with SAH, less natriuresis occurred and sodium balance was achieved more frequently.14,15 Thus, volume depletion and hyponatremia are preventable in patients treated with fludrocortisone. The most common adverse effect associated with fludrocortisone was hypokalemia, which was observed in up to 73% of patients.15 The length of therapy depends on the clinical course of the hyponatremia and the underlying pathology associated with CSW (Table 2). Once the underlying pathology is corrected, CSW is usually a transient condition that resolves within three to four weeks. Hence, long-term therapy is usually not needed.9 Case Outcome The case presented here illustrates the dilemma that clinicians face. The patient’s condition did not respond to fluid restriction, although his laboratory test results and presentation appeared to suggest SIADH. However, the fact that his hyponatremia continued to worsen with fluid restriction raised some questions. In addition, his fractional excretion of uric acid was persistently elevated. The patient also continued to have a high urine output. He was immediately given isotonic saline, keeping his net fluid balance positive. The serum sodium level started to improve, but he continued to require 3 L to 4 L of isotonic saline daily to keep his fluid balance between even and positive. Although there is no absolute certainty in a diagnosis of a clinical syndrome, the patient’s condition was diagnosed as probable CSW. He was eventually discharged with a serum sodium level of 140 mEq/L. Conclusion Hyponatremia in the setting of a central nervous system event is a diagnostic challenge to physicians. Both SIADH and CSW are likely etiologies, as they present with very similar biochemical profiles. Levels of natriuretic peptides and changes in fractional excretion of uric acid may help differentiate between the two conditions. The key difference is that SIADH is a euvolemic to mildly hypervolumic state, whereas CSW is a volume-depleted state. Unfortunately, the volume status is not always clinically apparent in every patient. It is important to consider CSW in addition to SIADH in patients who present with hyponatremia and an intracranial process. A correct and timely diagnosis is important in order to obtain a good outcome, because the two conditions are treated very differently. Disclosure Statement The author(s) have no conflicts of interest to disclose. Acknowledgment Katharine O’Moore-Klopf, ELS, of KOK Edit provided editorial assistance. References 1. Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med 2000 May 25;342(21):1581–9. 2. Betjes MG. Hyponatremia in acute brain disease: the cerebral salt wasting syndrome. Eur J Intern Med 2002 Feb;13(1):9–14. 3. Harrigan MR. Cerebral salt wasting syndrome: a review. Neurosurgery 1996 Jan;38(1)152–60. 4. Maesaka JK, Gupta S, Fishbane S. Cerebral salt-wasting syndrome: does it exist? Nephron 1999 Jun;82(2):100–9. 5. Peters JP, Welt LG, Sims EA, Orloff J, Neeham J. A salt-wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians 1950;63:57-64. 6. Schwartz WB, Bennett W, Curelop S, Bartter FC. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Am J Med 1957 Oct;23(4):529-42. 7. Sherlock M, O’Sullivan E, Agha A, et al. The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage. Clin Endocrinol (Oxf) 2006 Mar;64(3):250–4. 8. Palmer BF. Hyponatremia in patients with central nervous system disease: SIADH versus CSW. Trends Endocrinol Metab 2003;14(4):182–7. 9. Palmer BF. Hyponatraemia in a neurosurgical patient: syndrome of inappropriate antidiuretic hormone secretion versus cerebral salt wasting. Nephrol Dial Transplant 2000 Feb;15(2):262–8. 10. Singh S, Bohn D, Carlotti AP, Cusimano M, Rutka JT, Halperin ML. Cerebral salt wasting: truths, fallacies, theories, and challenges. Crit Care Med 2002 Nov;30(11):2575–9. 11. Chung HM, Kluge R, Schrier RW, Anderson RJ. Clinical assessment of extracellular fluid volume in hyponatremia. Am J Med 1987 Nov;83(5):905–8. 12. Decaux G, Namias B, Gulbis B, Soupart A. Evidence in hyponatremia related to inappropriate secretion of ADH that V1 receptor stimulation contributes to the increase in renal uric acid clearance. J Am Soc Nephrol 1996 May;7(5):805–10. 13. Berendes E, Walter M, Cullen P, et al. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage. Lancet 1997 Jan 25;349(9047):245–9. 14. Hasan D, Lindsay KW, Wijdicks EF, et al. Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage. Stroke 1989 Sep;20(9):1156–61. 15. Mori T, Katayama Y, Kawamata T, Hirayama T. Improved efficiency of hypervolemic therapy with inhibition of natriuresis by fludrocortisone in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg 1999 Dec;91(6):947–52.
Working with the Noncompliant Patient
Wednesday, 30 June 2010
Fred Kleinsinger, MD Spring 2010 - Volume 14 Number 1 Introduction For the Fall 2003 issue of The Permanente Journal,1 I wrote an article entitled “Understanding Noncompliant Behavior: Definitions and Causes”. It discussed the various underlying causes of more seriously noncompliant behavior (NCB) with the goal of understanding that noncompliance is not a unitary entity but has a differential diagnosis. Use of this differential diagnosis, it was stated, could lead to more effectively working with the noncompliant patient. The goal of this article is to offer the practicing clinician tools for working with the noncompliant patient. Background The initial article treated NCB as an aberration in the physician–patient alliance. In the few years since the publication of that article, there has been increased attention in the medical literature to this problem. The publications on this topic largely fall into two groups: articles on medication noncompliance, often dealing with related issues such as causes of noncompliance, and articles on disease-specific noncompliance, such as noncompliance in chronic pulmonary obstructive disease or asthma2 or noncompliance in patients with diabetes.3 What is apparent in most of these articles is that NCB is much more widespread than it was thought to be and that it has a serious, deleterious effect on health outcomes and medical costs. Osterberg and Blaschke4 wrote that “even clinical trials report average adherence rates of only 43 to 78 percent among patients receiving medication for chronic conditions” and that of “all medication-related hospital admissions in the United States, 33 to 69 percent are due to poor medication adherence, with a resultant cost of approximately $100 billion per year.” Cramer et al, reporting5 on a meta-analysis of compliance in diabetes, hypertension, and dyslipidemia, noted that “only 59% of patients [take] medication for more than 80% of the [prescribed doses] in a year.” Even in the case of serious and symptomatic disorders, such as acute myocardial infarction, a study6 has shown that as many as one in eight patients discontinue all three medications of the commonly prescribed combination of ?-blocker plus aspirin plus statin within one month of hospital discharge. These patients have an 80% higher chance of dying within the first year after discharge compared with patients taking all three classes of medication. It is apparent from these studies that NCB is epidemic and not just an aberration. NCB is likely one of the most common causes of treatment failure for chronic conditions, though this is not widely or consistently recognized. Noncompliance names a series of behaviors that fall on a continuum of severity, ranging from the trivial to the catastrophic. It would be a mistake to lump these together. Because I was unable to find a noncompliance rating scale in my literature review, I am proposing the tool shown in Table 1 to allow us to identify and compare differing intensities of NCB. My goal in this article is to focus on individual clinicians and their relationship with the noncompliant patients of greater degrees of severity (stages 2 and 3) in their clinical practice. Lesser degrees of NCB are more common and also detrimental to effective medical care. Given their frequency, these may require a systems approach rather than relying on the individual clinician. A detailed discussion of these approaches is beyond the scope of this article,7 but at least in terms of medication compliance, certain simple tools have been shown to be effective. These include simplifying medication regimens, using once-a-day dosing whenever possible, providing pillboxes for patients, using combination tablets when possible and appropriate, and using computerized tracking systems for prescription refills. The most effective systematic interventions that have been studied are multifaceted8 and of real but limited efficacy. McDonald et al conclude that “current methods of improving adherence for chronic health problems are mostly complex and not very effective, so that the full benefits of treatment cannot be realized.”9 Few articles in the literature deal with helping the physician with noncompliance. One useful article by Haynes et al10 makes a number of practical suggestions, including simplifying medication regimens, providing rewards and recognition for the patient’s efforts, and enlisting social support from family and friends. The same physician tools described in the following sections that are useful in more severe cases of NCB are also relevant to the milder degrees (stage 1 and early stage 2). Because so many of our patients are in this category, it can be difficult for the busy clinician to find time to deal with these issues. For some of these patients, however, identifying and countering a single and simple barrier to compliance can be readily accomplished. Dealing with Noncompliance General Principles In the modern clinical era, there has been a change in modes of physician–patient interaction and agreement. The more traditional authoritarian approach is transforming toward a collaborative partnership between patient and physician that is based on mutual goals and a shared understanding of problems and their potential solutions. A widely used current model is shared decision making,11 in which physician and patient, after discussion, agree on the nature of the problem in question and proposed steps toward its management. In a case discussion, Bodenheimer12 wrote, “A participatory relationship between patient and physician appears to be the most important factor promoting medication adherence” and that “the more actively the patient is involved, the higher the level of adherence and the greater the chance that the patient engages in healthy diet and exercise behaviors.” Trust between physician and patient is also a factor. Greater trust facilitates improved compliance.13 NCB can be understood as a breakdown in the physician–patient alliance and the implied or explicit contract between physician and patient. Understanding that this is a common phenomenon, and being aware of its possibility in a given clinical situation, is the first step toward dealing with this. The physician must realize the possibility that NCB is occurring in the given context with the particular patient—Sometimes this is apparent, as in the case of the patient who misses multiple appointments and who does not fill or refill prescriptions. Occasionally the patient will bring this up, but more often it requires a high index of suspicion and some detective work on the part of the physician. Given how common NCB is, it should be looked for in most cases of failure to meet treatment goals. How often do we add a third antihypertension medication when the patient in reality is not taking the first two regularly? The physician should raise this question with the patient in a problem-solving and nonjudgmental manner—“I see you haven’t refilled your antihypertension medication in six months. Are you having some problem with taking this medication?” Open-ended questions are best at first. Make sure that the physician and the patient have a common understanding of the importance of the medical problem in question, of the availability of effective treatments for this problem, and of the risks if the problem remains untreated or undertreated—This shared understanding is the foundation on which all treatment contracts are based. Start by asking how the patient understands the medical condition and why it needs treatment. Ask if the patient has any concerns or questions about the recommended treatments, lifestyle modifications, diagnostic tests, or follow-up and monitoring plans. Ask if there is an alternative approach that the patient has been using or considering. Allow time for this process, because whatever the patient tells you can be invaluable for tailoring your approach to improving compliance. It is sometimes hard for the physician to realize that there is an inherent power imbalance in the dynamic between physicians and patients. Physicians are comfortable in the world of medicine, whereas patients are often insecure and anxious in it. Physicians are at work, using professional training and experience to deal with other people’s problems, whereas patients are often worried about a problem that affects them immediately and personally. The medical profession enjoys high status, which can be intimidating For these reasons and others, if physicians do not work hard to be open and accessible to their patients’ ideas and thoughts, important information can be lost, handicapping our ability to understand what may be triggering noncompliance. Develop a shared understanding that the NCB itself is a mutual problem whose solution is vital to effective treatment—“I see that what we’ve been trying hasn’t worked that well. I’m concerned that this puts your health at risk. What do you think?” We want to avoid the power struggle that can develop when one party attempts to impose a viewpoint on another party. Reframing the noncompliance as a shared problem changes this dynamic. Build a more effective partnership (or therapeutic alliance) with the patient—Ask the patient for his or her analysis of the roots of the NCB. Ask what strategies the patient might suggest for addressing the problem. Again, open-ended, nonjudgmental questions can be very effective: • “What could I do differently to help you with this?” • “How could we approach this problem more effectively?” • “What are the obstacles that have prevented our dealing with this more successfully?” The very act of asking these questions can help reframe the situation from a more combative one to a more collaborative one. Be aware that guilt, shame, or a sense of failure is common when NCB is seriously threatening the patient’s health. Your open, nonaccusatory, and problem-solving stance will help defuse these negative emotions. Physician–Patient Conflict-Resolution Tools Though NCB is often not a direct manifestation of physician–patient conflict, communication tools that have proven effective in conflict situations can also be very useful in working with NCB. These tools have been developed primarily in nonmedical settings but can be very readily adapted for clinical use. Mirroring—Sometimes the simple act of mirroring what the patient says to you14 can defuse a difficult situation, even when you do not agree with the position the patient is taking. It also helps ensure that you correctly understand what your patient is telling you. By mirroring, I mean primarily verbal mirroring, in which the physician repeats back to the patient a summary or even a paraphrase of what the patient has been saying: Patient: I think this is all a waste of time. I’ll never lose weight, I hate sticking my finger all the time, and I’m too busy and stressed to eat the way I know I should be. Physician: I see that you’re very frustrated with how hard it’s been to live with your diabetes and that you feel that it’s been hard to do the finger sticks and to follow your diabetic diet. Did I get this right? Try to be as nonjudgmental and empathic as possible in your mirroring statement. Successful mirroring shows patients that they have been heard and understood, which is a prerequisite to moving toward new solutions. “I” Statements—Contrast in your mind the impact on the patient of the following two approaches to the same problem: Physician: You’re doing a very poor job controlling your diabetes. Don’t you know this could lead to serious complications? versus Physician: I’m worried that if your diabetes isn’t better controlled, you could develop some serious complications. Using statements that start with the word “I” and that express your genuine positions and concerns are much easier to hear and accept and foster a problem-solving versus a critical and blaming tone. Patients already often feel self-conscious and defensive when they are noncompliant. We want to break this cycle, and the physician’s working to sound more human and less authoritarian can enhance this possibility. Developing and Reinforcing Self-Efficacy—Many noncompliant patients have tried the best they can and feel like failures. Failure begets failure (just as success begets success) and stimulates feelings of despondency, depression, and denial. Breaking complex problems down into simpler components and then working on them one at a time and slowly can help combat this cycle of failure and defeat and encourages self-esteem and self-efficacy15–17: Physician: I see that it’s been very hard for you to do all the things you need to get your heart failure under control. Between now and our next visit, why don’t we focus on just one of the problem areas. We’ve identified that you’re having trouble taking your medications on time, following a low-salt diet, and doing regular exercise. Which would you like to focus on first? As physicians, we want the patient to answer “all of the above.” Yet the patient would not have become noncompliant if s/he had been able to accomplish this. We have to trust ourselves, in the possibility of slow progress over time, in the power of our strengthening relationship with the patient, and that this approach can facilitate the patient’s increasing sense of mastery and control. Some physicians may be concerned about potential medicolegal problems if the patient experiences an adverse consequence while being given permission to focus on limited areas of treatment at any one time. Good documentation of the treatment plan and its rationale make such problems unlikely. Enlisting Support—Most of our patients do not exist in a vacuum. They have their own formal and informal networks of support, including family, friends, associates, and other health care professionals. In many cases it can be helpful and appropriate for physicians to encourage patients to use other people in their lives to help improve compliance and self-care. In refractory cases of noncompliance, family members and friends can be enlisted in the campaign for better health. Patients can be asked, “Is there anyone in your life who could help you with this?” Could a spouse or partner or an adult child remind them to take their medications or to keep their appointments—without creating problems or tension in the relationship? This process must be with the consent of and under the control of patients; otherwise, we risk setting up a conflictual or codependent relationship. Patients can be asked to bring pertinent family members or friends to the medical appointment to discuss these issues. Sometimes these individuals will also have additional insights into the nature of the noncompliance problem that were not otherwise discoverable. In some health care settings, the physician has other colleagues who can be called on for assistance, including chronic-disease managers, case managers, nurse practitioners, and behavioral-medicine specialists. These individuals may have more time available per encounter than the physician, and their motivational and teaching skills can be extremely helpful in complementing the physician’s approach. Physicians themselves often feel stymied and frustrated in working with highly noncompliant patients and can benefit from discussions with colleagues, consultation with behavioral-medicine specialists, or by making use of a variety of practice-support settings such as Balint groups, should these be available. Approaches to Specific Causes of Noncompliant Behavior In the first section of this article, I described and identified specific causes that sometimes underlie NCB. There are targeted approaches to NCB that are based on the suspected etiology of these behaviors that can supplement the more general approaches just described. Denial Denial, as a defense from the stress and worry of living with a chronic condition, can have a positive value. However, when denial interferes with getting necessary care, it can become a common cause of NCB. Fear often underlies more pronounced forms of denial. Gently inquiring how the patient understands his or her illness, its likely course, its possible complications, or the effects of treatment can lead to a beneficial discussion in which the concept of denial can be introduced if it seems relevant. In my experience, talking about denial in a nonjudgmental way often leads to a useful and clarifying discussion. Enlist patients’ support in working with their denial. Most patients have heard of the term denial and can be asked if they think this is playing a role in how they are dealing with their disorder. Frontal assaults on denial, however (“You’ll die if you don’t take better care of yourself”), feed and strengthen the denial. Feeling overwhelmed also breeds denial. Identifying these feelings and simplifying medical regimens whenever possible (see the “Developing and Reinforcing Self-Efficacy” section earlier in this article) can lessen the impetus to denial as well. Depression Part of the experience of being depressed is the loss of optimism, of self-worth and self-efficacy, and a lowering of energy. These can all interfere with chronic illness care and lead to NCB. Depressed patients are three times more likely to be noncompliant with medical treatment recommendations than are nondepressed patients.18 Because depression itself is common, especially among the chronically ill, the clinician should be alert to this possibility and use depression screening tools such as the nine-item depression scale of the Patient Health Questionnaire (PHQ9) (Pfizer, Inc, New York) (and others) readily with noncompliant patients. Treatment of depression may well facilitate medical compliance. Dementia Dementia, especially early in its onset, can both be nonapparent to the clinician and yet subtly impair the skills needed for medical compliance.19–21 In select patients with NCB, use of dementia screens like the Mini-Mental Status Exam (Psychological Assessment Resources, Lutz, FL) may reveal unsuspected subtle cognitive impairments that interfere with compliance. When this is recognized, the clinician, in collaboration with the patient, can seek the assistance of other persons or agencies that can assist with care, as well as with undertaking the evaluation and potential treatment of the cognitive decline. Cultural Issues The greater the discrepancy between the cultural background of the physician and the patient (and the patient’s family), the greater the likelihood for miscommunication and NCB. Cultural differences can affect more than the understanding of the meaning and causes of illness. They also affect one’s understanding of how symptoms or illnesses should be managed and how physician and patient should communicate. Dealing with these crosscultural issues is beyond the scope of this article, but the issue has been widely discussed in the medical literature. Recommended general approaches include: Being aware of the potential impact of cultural issues on the treatment process. Being willing to engage the patient in a collaborative and nonjudgmental manner regarding these issues. Seeking clarification regarding these issues from the medical literature, from programs aimed at understanding cultural diversity in medicine, and from colleagues with expertise in these issues. Drug or Alcohol Dependence Misuse of alcohol or recreational drugs impairs compliance.22,23 Screening for these problems is advisable for patients with NCB and can be rapidly accomplished using the CAGE tool for alcohol abuse and by asking the patient about drug use. Asking, “What drugs have you ever used occasionally?” may be helpful. Remember that alcohol and drug abuse is found in all sectors of the population. Whether identifying and treating substance abuse improves compliance has not been thoroughly studied. Because uncovering substance abuse is generally considered to be beneficial in its own right, it certainly makes sense to do this when evaluating NCB even if we cannot prove its benefits in this arena at present. Counseling the patient regarding these disorders and making appropriate referrals to chemical-dependence programs may affect NCB and is worth doing for many other reasons. Cost of Treatment When patients cannot afford their medical care, as is all too common in the US given our lack of universal health care and the high costs of treatment, this is not, technically, noncompliance. The economic barriers to medical care are the primary factor here, not the actions or inactions of a given patient. Having stated this, I must add that there are also many cases in which the relative affordability of treatment affects degrees of compliance in patients who are able to pay at least some of their medical expenses. In a study of Medicare enrollees completed before Medicare Part D was implemented, 13% of Medicare patients (and 29% of disabled Medicare patients) reported cost-related noncompliance.24 Asking patients if the cost of treatment is a problem for them should be done widely in evaluating NCB. If this proves to be the case, strategies include using generic and less-expensive medications when possible and reducing visit frequency for patients with stable diseases. Patients can be referred for various forms of financial assistance that may be available as well. Summary and Conclusions Using the diagnostic and therapeutic approaches outlined in this article, reviewed in Table 2, can improve your success rate in dealing with NCB and can reduce both your and your patients’ tension and frustrations. It can help align you and your patient toward a shared framework and collaboration rather than blaming and mistrust. Being open, nonjudgmental, and inquisitive can only be beneficial here and may well reveal causes of noncompliance that are not mentioned in this article. A sample dialog with a stage 2 noncompliant patient using communication tools described here may be viewed on The Permanente Journal Web site at: http://xnet.kp.org/permanentejournal/spr10/appendix/WorkingWithTheNoncompliantPatient.pdf Taking a holistic and strategic approach to NCB can also help the physician reframe these encounters, so that they become a stimulating therapeutic challenge. Being thoughtful, patient, and believing yourself in the possibility of long-term incremental change in NCB can help develop your own self-esteem and self-efficacy in working with these challenging and difficult patients. Disclosure Statement The author(s) have no conflicts of interest to disclose. Acknowledgment Katharine O’Moore-Klopf, ELS, of KOK Edit provided editorial assistance. References 1. Kleinsinger F. Understanding noncompliant behavior: definitions and causes. Perm J 2003 Fall;7(4):18-21. 2. Bourbeau J, Bartlett SJ. Patient adherence in COPD. Thorax 2008 Sep;63(9):831–8. 3. Leichter SB. Making outpatient care of diabetes more efficient: analyzing noncompliance. Clinical Diabetes 2005 Oct;23(4):187–90. 4. Osterberg L, Blaschke T. Adherence to medication. N Engl J Med 2005 Aug 4;353(5):487–97. 5. Cramer JA, Benedict A, Muszbek N, Keskinaslan A, Khan ZM. The significance of compliance and persistence in the treatment of diabetes, hypertension and dyslipidaemia: a review. Int J Clin Pract 2008 Jan;62(1):76–87. 6. Ho PM, Spertus JA, Masoudi FA, et al. Impact of medication therapy discontinuation on mortality after myocardial infarction. Arch Intern Med 2006 Sep 25;166(17):1842–7. 7. O’Connor PJ. Improving medication adherence: challenges for physicians, payers, and policy makers [editorial]. Arch Intern Med 2006;166(17):1802–4. 8. Roter DL, Hall JA, Merisca R, Nordstrom B, Cretin D, Svarstad B. Effectiveness of interventions to improve patient compliance: a meta-analysis. Med Care 1998 Aug;36(8):1138–61. 9. McDonald HP, Garg AX, Haynes, RB. Interventions to enhance patient adherence to medication prescriptions: scientific review. JAMA 2002 Dec 11;288(22):2868–79. Erratum in: JAMA 2003 Jun 25;289(24):3242. 10. Haynes RB, Ackloo E, Sahota N, McDonald HP, Xao X. Interventions for enhancing medication adherence. Cochrane Database Syst Rev 2008 Apr 16;(2)CD000011. 11. Emanuel EJ, Emanuel LL. Four models of the physician-patient relationship. JAMA 1992 Apr 22–29;267(16):2221–6. 12. Bodenheimer T. A 63-year-old man with multiple cardiovascular risk factors and poor adherence to treatment plans. JAMA 2007 Nov 7;298(17):2048–55. 13. Thom DH, Ribisl KM, Stewart AL, Luke DA. Further validation and reliability testing of the Trust in Physician Scale. The Stanford Trust Study Physicians. Med Care 1999 May;37(5):510–7. 14. Clabby J, O’Connor R. Teaching learners to use mirroring: rapport lessons from neurolinguistic programming. Fam Med 2004 Sep;36(8):541–3. 15. Sobel DS. Rethinking medicine: improving health outcomes with cost-effective psychosocial interventions. Psychosom Med 1995 May–Jun;57(3):234–44. 16. Marks R, Allegrante JP, Lorig K. A review and synthesis of research evidence for self-efficacy-enhancing interventions for reducing chronic disability: implications for health education practice (part I). Health Promot Pract 2005 Jan;6(1):37–43. 17. Marks R, Allegrante JP, Lorig K. A review and synthesis of research evidence for self-efficacy-enhancing interventions for reducing chronic disability: implications for health education practice (part II). Health Promot Pract 2005 Apr;6(2):148–56. 18. DiMatteo MR, Lepper HS, Croghan TW. Depression is a risk factor for noncompliance with medical treatment: meta-analysis of the effects of anxiety and depression on patient adherence. Arch Intern Med 2000 Jul 24;160(14):2101–7. 19. Stilley CS, Sereika S, Muldoon MF, Ryan CM, Dunbar-Jacob J. Psychological and cognitive function: predictors of adherence with cholesterol lowering treatment. Ann Behav Med 2004 Apr;27(2):117–24. 20. Stoehr GP, Lu SY, Lavery L, et al. Factors associated with adherence to medication regimens in older primary care patients: the Steel Valley Seniors Survey. Am J Geriatr Pharmacother 2008 Dec;6(5):255–63. 21. Arlt S, Lindner R, Rösler A, von Renteln-Kruse W. Adherence to medication in patients with dementia: predictors and strategies for improvement. Drugs Aging 2008;25(12):1033–47. 22. Bryson CL, Au DH, Sun H, Williams EC, Kivlahan DR, Bradley KA. Alcohol screening scores and medication nonadherence. Ann Intern Med 2008 Dec 2;149(11):795–804. 23. Golin C. Drinking and drugs: when is enough too much? [editorial]. Ann Intern Med 2008 Dec 2;149(11):830–2. 24. Soumerai SB, Pierre-Jacques M, Zhang F, et al. Cost-related medication nonadherence among elderly and disabled medicare beneficiaries: a national survey 1 year before the medicare drug benefit. Arch Intern Med 2006 Sep 25;166(17):1829–35.
Health Care Delivery Performance: Service, Outcomes, and Resource Stewardship
Friday, 02 July 2010
Michelle Cowing, PhD; Carrie M Davino-Ramaya, MD; Krishnan Ramaya, PhD; Joseph Szmerekovsky, PhD Fall 2009 - Volume 13 Number 4 Abstract As competition intensifies within the health care industry, patient satisfaction and service quality are providing the evidentiary basis for patient outcomes. We propose a conceptual model of three interrelated areas, service, health outcomes, and resource stewardship, all affected by the clinician-patient relationship. Our model considers the perspectives of the health care organization, the clinician, and the patient to define a more comprehensive measure of health care delivery performance. Research and managerial aspects, including implementation, are discussed. Introduction Managed health care in the US, intended to reduce the cost of health benefits while improving the quality of care, has grown rapidly during the 21st century, leading to an increasingly competitive health care industry. As competition intensifies, patient satisfaction, service quality, and efficient resource management are providing the evidentiary basis for measuring patient, clinician, and organizational outcomes. With emphasis on “quality outcomes,” it is becoming increasingly critical for health care organizations to develop and implement a sound strategy for providing effective care that is appealing to patients and focuses on controlling costs. Health care as a whole faces the challenges of attracting and retaining patients and talented employees while delivering consistently effective and efficient care. To that end, we propose a conceptual model of three critical and interrelated outcomes of health care delivery: service, quality, and resource stewardship. The model explicitly recognizes the perspectives of the health care organization as well as the perspectives of the clinician and the patient, and it defines appropriate and comprehensive measures of health care delivery performance. Although a growing body of evidence links a clinician-patient relationship defined by effective communication with improved patient outcomes, our model uniquely takes into account the psychosocial components of both the clinician and the patient while closely linking and integrating a business-management model of health care delivery for which there is a paucity of research in the current literature. Through the explicit recognition and eventual empirical examination of the relationships among these critical elements, the model will allow health care organizations to explore the impact of various operational improvement strategies. Determinants of Health Care Performance Assessing the quality of care is not new in health care; the rapid growth of the managed-care industry in the US has lead to a variety of definitions and perceptions of quality. Today, several well-established agencies and organizations address improving health care quality and patient safety through a process known as continuous quality improvement. Organizations such as the Agency for Healthcare Research and Quality,1 the National Committee for Quality Assurance (NCQA),2 and the Joint Commission, to name a few, have emerged with the specific intent to support quality, safety, efficiency, and effectiveness of health care in the US. These organizations define or assist in defining nationally derived measures or standards that are used to assess the quality of health care. The NCQA continues to raise the bar on health care quality. In early 2008, it launched a new version of its Physician Practice Connections program designed to assess how medical practices are functioning as patient-centered medical homes. The new Physician Practice Connections--Patient-Centered Medical Home emphasizes the systematic use of patient-centered, coordinated care-management processes. Although likely relevant to our proposed model, that new program3 is beyond the scope of this article. Clearly, as health care competitive dynamics continue to evolve, it is no longer sufficient to define health care performance in terms of clinical outcomes alone. The inclusion of patient satisfaction is fast becoming an important dimension because the notion of consumer-driven health care increasingly applies to patient choice in the health care industry.4–7 Figure 1 explicitly defines the broad determinants of performance necessary to adequately assess the multiple dimensions of health care delivery performance. Items listed in Box A of the figure are intended to capture those aspects of performance that are currently defined and emphasized in the industry as indicators of quality. These measures include the more technical and objective guidelines and standards used to assess clinical and health outcomes. The items in Box B of the figure are concepts that represent an opportunity for the health care industry to more effectively integrate into the process or functional side of service quality. Relevant process-related determinants of quality include patient satisfaction and perception of service delivery (by patient and clinician). These are typically a function of subjective assessments that are based on the nature of interactions with staff, nature of communication with clinicians, degree of personalized care, accessibility of care, and responsiveness and timeliness of care. Although inherently more complex to define and measure, these concepts may play an essential role in measuring service quality in health care today. The challenge for health care organizations is to define and track comprehensive measures of health care delivery performance that include elements from both Box A and Box B. As shown in Figure 1, Box A and Box B items are affected by the design of the health care delivery system. Typical design elements include how processes and procedures are developed and implemented; what clinical standards are in place and enforced; and clinic accessibility in terms of hours, location, available transportation, insurance, coverage/copays, the level at which the clinic is staffed, how staff are trained, and how staff are scheduled. In other words, a clinic can affect both its outcome and process measures of performance by changing its design elements. For example, patient satisfaction might increase if a clinic were staffed at a higher level. Of course, such a design change would have to be evaluated in conjunction with an assessment of the cost of such a change. Figure 1 also depicts the important feedback between Box B process-related measures and Box A outcome measures. It is well documented that patients who perceive an encounter with their clinician to be patient-centered show better recovery and better emotional health and need fewer diagnostic tests and referrals up to two months after the baseline visit.8 In general, if patients are satisfied with clinician-patient interaction, they are likely to be more compliant with their treatment plan, to understand their role in the recovery process, and to follow through with the recommended treatment. Subsequently, improved health outcomes are more likely. Thus, our model recognizes the interdependence of process and outcome measures. Health Care Delivery Triad and Performance To appropriately define and fully understand relevant performance measures in the health care industry, it is necessary to consider each of the three key players or entities in the service triad: the health care organization, the clinician (team of physicians, nurses, medical assistants, and office staff), and the patient. Each of these three entities has a unique but interrelated perspective on the needs associated with health care performance. Figure 2 defines each player in the health care encounter. By considering the perspectives and associated needs of each of these players, we can derive a more comprehensive set of performance measures appropriate for evaluating health care. The development and application of triads in health care is not a new concept. As pointed out by Glickman et al,9 Avedis Donabedian’s triad, with its structure-process-outcomes framework, provided a solid foundation in which to think about quality-improvement efforts, “... but his view of structure needs to be updated to account for current tools and management capabilities that drive quality improvement.”9 In their work, Glickman et al discuss key elements of organizational attributes from a management perspective in an effort to develop a definition of structure for transforming quality-improvement initiatives. With respect to health care organizations, for example, a number of indicators related to responsible resource stewardship may be of primary concern. From the health care organization perspective, measures related to the effective and efficient use of its valuable and scarce resources are critical to assessing performance. Specific measures related to costs, times, and rates of service would define operational efficiency, whereas various clinical performance measures would indicate operational effectiveness. Risk-management costs and benefits would also fall under the organization’s need for responsible resource stewardship. From the patient’s perspective, we are primarily interested in defining and capturing needs associated with both subjective and objective indicators of “satisfaction” with the care provided. As noted earlier in the “Determinants of Health Care Performance” section, patient satisfaction is based on a range of characteristics and experiences, including subjective perception of the service and care, the degree of personalization of care, the expectations and psychosocial needs of the patient, and the ultimate health outcome. Because of the established link between patient satisfaction and clinician satisfaction,10,11 our model explicitly includes clinician needs related to job satisfaction and organizational support. In fact, we believe that clinician satisfaction is also tied to the organizational need for resource stewardship. Clinician satisfaction is based on factors such as clinicians’ subjective perception of their ability to deliver quality care and whether there are adequate organizational support and resources for them to effectively perform their jobs. Conceptual Model of Health Care Delivery Performance We now expand on the health care delivery triad by considering the interrelationships among the three members of the triad. Adapted from the general service management literature defining a service encounter triad,12 we consider the possible ways in which the perspective or needs of each party supports or detracts from the needs of the other parties. In fact, the performance measures derived from each perspective are, in general, functions of the other perspectives and dimensions of performance. They are also dependent on the design of the health care delivery system and on other organizationwide factors. Figure 3 displays these interactions among the triad members and resulting performance and quality measures. We will discuss each of the three pairings or relationships in turn. The primary consideration when evaluating the relationship between health care organization and patient is the impact of the operational design of the health care delivery system. For example, the design defines issues of accessibility, process structures, procedures followed versus required, ratio of staff to patients, degree of reliance on clinical practice guidelines, etc. Clearly, the specification of these parameters is significant to the organization’s measures of resource stewardship and also to the patient’s measures of satisfaction. These measures of resource stewardship and patient satisfaction, then, are clearly not independent. It is, in fact, quite possible that they are at times in direct conflict. For example, a lower ratio of staff to patients would help the organization keep costs low (better operational efficiency), but it may result in longer patient wait times or less responsive service and therefore lower patient satisfaction. However, the reverse is also possible. Wanless13 has identified a number of specific organizational benefits that can occur as the result of increased patient satisfaction, including specific operational, financial, and marketing benefits. Consider next the relationship between the health care organization and the clinicians (team of physicians, nurses, assistants, and staff). We define the nature of this relationship in terms of the nature and degree of support and resources provided by the organization to clinicians and its expectations of the clinicians. These variables are, in general, set or defined by the organization (ie, the administration thereof) and have implications for the culture of the organization, incentives (formal or informal) for clinicians, degree of time or other resource pressures on medical staff, scheduling (level and pace), and training. These in turn affect clinician satisfaction as well as operational efficiency and effectiveness. As in the organization–patient relationship, how these resource and support variables are set may result in tradeoffs when viewed from the organization’s perspective versus the clinician’s perspective. Tight scheduling may improve the organization-level operational efficiency measures but may create conditions under which clinicians feel less able to deliver personalized care, which may in turn lower clinician satisfaction. To highlight this point, a 2009 article14 in the journal Academy of Management Perspectives discussed health care innovations that often lead to implementation failure because of the perceived notion that the innovation is an “additional and distinct activity from their core task of patient care delivery.” Finally, we consider the clinician-patient relationship. We explore this relationship in terms of the nature and effectiveness of communication and level of patient advocacy (real or perceived). We know from empirical studies that the nature of this relationship and interaction is significant in determining patient satisfaction.15–20 Commonly cited reasons for quality of care complaints include the following: the clinician did not make eye contact the clinician did not sit down the clinician did not seem to listen the clinician seemed rushed and/or uncaring. Empirical studies have shown that health care organizations offering higher levels of patient-centered care--that is, those in which interactions are characterized by better patient–clinician communication, such that the clinician showed more empathy and allowed for the patient’s perspective--see better recovery rates, better emotional health, fewer follow-up tests and referrals, and fewer malpractice lawsuits.8,21–26 Thus, it appears that there is a direct association between a patient’s observation of poor verbal and nonverbal communication skills on the part of the clinician and the patient’s negative assessment of the quality of care received. Conversely, more favorable personal interactions result in higher patient satisfaction and quality-of-care assessments. The Clinician-Patient Relationship Of the three dyadic relationships defined among our health care delivery triad, it is the definition of the clinician-patient relationship that we find particularly critical for understanding and improving the quality of health care delivery. This relationship, however, is perhaps the least well defined. Here we identify a number of characteristics that threaten the effectiveness of this relationship. Among a multitude of challenges faced by health care organizations, the ability to recognize and successfully manage barriers to effective clinician-patient interactions will ultimately serve as determinants of success. By its very nature, the clinician-patient relationship is inherently complex and thus difficult to reliably measure. To begin with, the interaction is in real time and subjectively experienced. For example, factors such as expectations, personalities, anxieties, and external conditions, affect both patient and clinician perception in their assessment of whether or not a specific clinician-patient interaction resulted in effective communication and/or patient advocacy. Attempting to meaningfully measure and interpret results, then, will clearly be difficult. The interaction can be further strained or constrained because of the nature of the subject of discussion during the office visit. Health care and health-related concerns are inherently personal and are often coupled with patient uncertainty and anxiety. Thus, the subject may be difficult for the patient to talk about, resulting in uncomfortable communication or even insufficient information from which the clinician must try to make an appropriate diagnosis. Studies have shown that patients may not express their chief physical complaint at the onset of the clinician-patient encounter. Use of open-ended questions, however, can help elicit the chief complaint and is a proven approach for drawing out the most pressing health issues or concerns.26–29 The time for use of such questions may not be available in a routine visit. It is also possible that at times, the clinician’s agenda and the patient’s agenda are at odds. For instance, the clinician needs to gather specific information from the patient (eg, current medications, most recent examinations and procedures), whereas the patient may have the need or desire to discuss a wide range of life and health concerns with the clinician. The resulting conversation would likely seem frustrating and unsatisfying to both clinician and patient. Further compounding the challenges of this relationship is the fact that traditional clinician skills and competencies (ie, technical medical training) are often at odds with the personal skills and competencies required for sensitive, effective communication across a wide range of patients. Finally, it is conceivable that organizational requirements for efficiency, particularly important for financial viability in a highly competitive health care industry, may not be consistent with requirements for facilitating personalized, empathetic clinician-patient interactions. Implications for Policy and Practice As part of a highly competitive industry, health care organizations and their administrators must adopt a more comprehensive view of health care delivery quality. Initiatives to improve health care quality must address patient satisfaction in addition to more traditional quality indicators. Further, it is the clinician-patient relationship that is central to patient perception of quality and satisfaction with the care. Although this relationship is inherently complex, the recognition of the determinants of this complexity and the creation of strategies for effectively managing these are essential challenges for successful health care organizations. Health care organizations must also better define and track appropriate measures of patient satisfaction. It is possible that current survey tools are not adequate for effectively capturing the scope and nature of information necessary for identifying the underlying determinants of patient satisfaction and how elements of the health care delivery system impact these. Finally, it is likely that current models of health care delivery are not optimal for the new age of health care competition. Redesign of processes and organizations will be required to overcome barriers to service quality improvement and to allow for more balanced health care delivery. Our work to date defines factors that are essential for a more comprehensive assessment of health care quality. It provides a conceptual framework from which to better understand the relevant determinants of quality, how they are interrelated, and how they relate to the process design characteristics. The need to demonstrate that these relationships are linked to operational aspects of the health care delivery system warrants further investigation that would combine both quantitative and qualitative dimensions. Through empirical validation of our model of health care delivery performance, we intend to quantify the impact of alternative health care delivery-system design features on service quality and patient satisfaction. The resultant tool will allow health care organizations to systematically evaluate and implement a range of potential operational improvement strategies. Disclosure Statement The author(s) have no conflicts of interest to disclose. Acknowledgment Katharine O’Moore-Klopf, ELS, of KOK Edit provided editorial assistance. References 1. What is AHRQ? [monograph on the Internet]. Rockville, MD: Agency for Healthcare Research and Quality; 2002 Feb [cited 2009 Sep 21]. AHRQ Publication No. 02-0011. Available from: www.ahrq.gov/about/whatis.htm. 2. NCQA news release: NCQA program to evaluate patient-centered medical homes [monograph on the Internet]. Washington, DC: National Committee for Quality Assurance; 2008 Jan 8 [cited 2009 Sep 21]. Available from: www.ncqa.org/tabid/641/Default.aspx. 3. What is HEDIS? HEDIS and Quality Compass [monograph on the Internet]. Washington, DC: National Committee for Quality Assurance; 2009 [cited 2009 Sep 21]. 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Continuity, care, and commitment: the course of patient–clinician relationships. Ann Fam Med 2004 Sep–Oct;2(5):388–90. 16. Mayberry RM, Nicewander DA, Qin H, Ballard DJ. Improving quality and reducing inequities: a challenge in achieving best care. Proc (Bayl Univ Med Cent) 2006 Apr;19(2):103–18. 17. Dugdale DC, Epstein R, Pantilat SZ. Time and the patient–physician relationship. J Gen Intern Med 1999 Jan;14 Suppl 1:S34–S40. 18. Fan VS, Burman M, McDonell MB, Fihn SD. Continuity of care and other determinants of patient satisfaction with primary care. J Gen Intern Med 2005 Mar;20(3):226–33. 19. Beach MC, Inui T; Relationship-Centered Care Research Network. Relationship-centered care research network. A constructive reframing. J Gen Intern Med 2006 Jan;21 Suppl 1:S3–8. 20. O’Malley AS, Forrest CB. Beyond the examination room: primary care performance and the patient–physician relationship for low-income women. J Gen Intern Med 2002 Jan;17(1):66–74. 21. 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Image Diagnosis: Pulmonary Embolism, Radial Head Fracture, Abdominal Aortic Aneurysm
Friday, 11 February 2011
Gus M Garmel, MD, FACEP, FAAEM Fall 2008 - Volume 12 Number 4 Pulmonary Embolism Figure 1. Axial view from a computed tomography (CT) angiogram which beautifully demonstrates a large saddle pulmonary embolus in a previously healthy female age 33 years who presented to the Emergency Department following a syncopal episode. She was not pregnant, and had mild chest pain, dyspnea, tachycardia, and tachypnea, which were not present before her episode. Figure 2. (same patient) CT angiogram demonstrating a large branching clot consistent with a pulmonary embolism. Figure 3. Compression ultrasound demonstrates a patent popliteal artery (A) in both images. A clot can be seen in the popliteal vein (V), which does not collapse during compression (right-sided image). Acknowledgments Dr Garmel would like to thank Bruce Wollman, MD; John Rego, MD; and Diane Craig, MD, for their assistance selecting the most illustrative images for this interesting case, as well as for their participation in the care of this challenging patient. Radial Head Fracture The patient presented to the urgent care clinic after trauma to the upper extremity. Figure 1. Lateral view of an elbow, in which you can easily see a posterior fat pad (never normal) and an anterior “sail sign.” Together, these represent a relatively large hemarthrosis around the elbow joint, suggestive of a fracture. On close inspection, a cortical disruption and small depression of the radial head is apparent. There is also slight elevation of the supinator line due to the hemarthrosis present, although this finding is much more subtle and less specific. Abdominal Aortic Aneurysm Figure 1. Abdominal computed tomography (CT) scan with IV contrast demonstrates a leaking abdominal aortic aneurysm (AAA). The light arrow points to contrast within the lumen of the abdominal aorta. The dark arrow points to the outer walls of the abdominal aorta. At the level of the kidneys, the abdominal aorta is always found directly on top of the spine. K = kidney, B = spine (vertebral body), L = liver Figure 2. Normal abdominal CT scan.