Accuracy of ICD-9-CM codes in detecting community-acquired pneumococcal pneumonia for incidence and vaccine efficacy studies

Studies have used medical record discharge data as coded by the International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) to estimate pneumococcal pneumonia incidence and vaccine efficacy. However, the accuracy of coding data to identify laboratory-confirmed pneumococcal pneumonia is not known. With the use of information collected in Ohio for a community-based pneumonia incidence study, the authors calculated the sensitivities, specificities, positive predictive values (PPV), and negative predictive values (NPV) of specific codes for pneumococcal pneumonia among hospitalized patients with community-acquired pneumonia. Sensitivities of the most common ICD-9-CM codes listed in the first five positions for patients with laboratory-confirmed pneumococcal pneumonia were 58.3% (code 481.0, pneumococcal pneumonia), 20.4% (38.0, streptococcal septicemia), 19.2% (38.2, pneumococcal septicemia), 15.0% (518.81, respiratory failure), 14.2% (486.0, pneumonia, organism unspecified), and 11.3% (482.3, streptococcal pneumonia). Using the first five listed ICD-9-CM codes rather than just the first listed code increased sensitivity without causing substantial change in specificity, PPV, and NPV. Sensitivity, PPV, and NPV of individual and groups of codes varied with different case definitions of pneumococcal pneumonia. Incidence and vaccine efficacy studies with the ability to validate diagnoses by medical chart review can use a combination of many ICD-9-CM codes to maximize sensitivity. However, without the ability to review medical charts, researchers must carefully decide which codes would best suit their studies.     

Ace inhibitors: treatment of congestive heart failure

Nasal passage geometry was measured by acoustic rhinometry in 8 healthy medical students (5 males and 3 females, 21-29 years old; mean age 24 years) after 6 min in different postures of head and body. The minimum cross-sectional area (A-min) and volume between the nostril and 7 cm posteriorly were measured on both sides. When changing from sitting to horizontal the total airway dimension (i.e., the sum of A-min for the two sides) decreased by about 16% (Mean +/- SD = 0.19 +/- 0.14 cm2), and when standing up it increased by about 12% (0.14 +/- 0.13 cm2). A-min seemed more sensitive than volume to detecting postural changes. Including the variation between the cavities, the coefficient of variation (CV = SD/Mean) for area was 24.8 +/- 6.7 and for volume 22.4 +/- 6.4 for the 8 subjects. For the total nasal airway passage the corresponding figures were 12.9 +/- 3.9 and 10.9 +/- 5.5. These figures are considerably higher than for subjects measured only in the sitting position under comparable circumstances. In conclusion, our findings indicate a composite response of the nasal cavity mucosa to both systemic (hydrostatic) and local conditions, probably induced by vascular and cutaneous reflexes. These factors must be taken into account in studies of environmental, clinical, and pharmacological conditions.     

Accuracy of ICD-9-CM coding for the identification of patients with acute ischemic stroke: effect of modifier codes

BACKGROUND AND PURPOSE: Discharge ICD-9-CM (International Classification of Diseases, 9th Revision, Clinical Modification) codes have been used to identify patients with acute stroke for epidemiological, quality of care, and cost studies. The aim of this study was to determine if the accuracy of the primary ICD-9-CM codes for ischemic stroke is improved by modifier codes and how specific codes reflect stroke subtype diagnoses. METHODS: Available hospital charts for all patients discharged from a single hospital between May 1995 and June 1997 with ICD-9-CM codes 433 (occlusion and stenosis of precerebral arteries), 434 (occlusion of cerebral arteries), or 436 (acute but ill-defined cerebrovascular disease) listed in the first position were reviewed. The primary discharge diagnosis was verified, and a presumed stroke subtype was assigned on the basis of information provided in the medical record. RESULTS: Charts were available for 175 of the 198 identified patients (88%). Of these, 61% had an acute ischemic stroke (code 433, 4%; 434, 82%; 436, 79%) with the remaining patients having other conditions. Of the 130 patients with a modifier code indicating cerebral infarction, 79% had an acute stroke; of the 45 patients with a modifier code indicating an absence of cerebral infarction, 7% had acute stroke (sensitivity, 0.97; specificity, 0.60). The codes with the highest proportions of ischemic stroke cases were 434.11 (embolic occlusion of cerebral arteries with infarction, 85%), 434.91 (unspecified occlusion of precerebral arteries with infarction, 82%), and 436 (79%), with a combined sensitivity of 0.81 and specificity of 0.90. On review, 73% of patients with code 434.11 had embolic strokes, and 47% of those with code 436 had an identified stroke cause. Of patients with code 434.91, 39% had stroke of uncertain cause, 25% "lacunar," 17% atherothrombosis, and 15% embolism. CONCLUSIONS: Despite the use of modifier codes, 15% to 20% of patients with the indicated primary ICD-9-CM codes have conditions other than acute ischemic stroke. Although the proportion of patients with acute stroke increased from 61% to 79% with the use of modifier codes, the inclusion of modifier codes did not have an appreciable effect on the accuracy of the coding if patients with code 433 are excluded. Assignment of presumed ischemic stroke subtype is particularly inaccurate.     

Preventing congestive heart failure

The morbidity, mortality and health care costs associated with congestive heart failure make prevention a more attractive public health strategy than treatment. Aggressive management of etiologic factors, including hypertension, coronary artery disease, valvular disease and excessive alcohol intake, can prevent the left ventricular remodeling and dysfunction that lead to heart failure. Early intervention with angiotensin converting enzyme inhibitors in patients with chronic left ventricular dysfunction can prevent, as well as treat, the syndrome. Several intervention strategies in patients with acute myocardial infarction can slow or prevent the left ventricular remodeling process that antedates congestive heart failure. The primary care physician must be alert to the need for aggressive intervention to reduce the burden of heart failure syndrome on the patient and on society.     

Medical therapy of chronic heart failure. Role of ACE inhibitors and beta-blockers

Heart failure has long been considered to have a progressive downhill course leading inexorably to an early demise. This course often occurs silently, in the absence of any obvious cardiac insults. The reason for this is a combination of cell loss, myocyte dysfunction, impaired energetics, and pathologic remodeling of the chamber. Improved clinical outcome should result from strategies that reduce the biologic signals responsible for myocyte growth, dysfunction, and loss and chamber remodeling. Clinicians should no longer attempt to treat chronic heart failure with pharmacologic growth and remodeling process. In time, it may be possible for the clinician to view the treatment of heart failure largely as a matter of improving the biologic function of the myocardium.     

Amiodarone in congestive heart failure

Originally developed as an antianginal agent, amiodarone was soon found to have antiarrhythmic properties and to be a non-competitive inhibitor of alpha and beta-adrenergic receptors. Many trials studying the use of amiodarone in patients with heart failure have now been performed and are reviewed in this article. The trials appear to show that amiodarone possesses significant antiarrhythmic activity, even in heart failure patients. The drug appears to be well tolerated and proarrhythmia is uncommon. Based on the findings of a large Argentinian randomised trial (GESICA) and the Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHF STAT), it would appear there is a role for amiodarone in patients with non-ischaemic cardiomyopathy, but prospective studies are required to confirm this. The benefit of amiodarone in patients with non-ischaemic cardiomyopathy might be related to the beta-blocking effect that is seen with the use of conventional beta-blockers. Further studies, including the Sudden Cardiac Death Heart Trial (SCD HeFT), should help determine the role of amiodarone in heart failure patients.     

Hemorrhagic ascites due to congestive heart failure

Ascites due to congestive heart failure (CHF) is characteristically serous in gross appearance. Although hemorrhage into ascites commonly indicates a malignant or inflammatory cause, cirrhosis of the liver is a well known cause of bloody ascites. We report a case of hemorrhagic ascites due to biventricular congestive heart failure in which workup for other causes was negative and hemorrhage cleared after 4 months. In as much as the mechanism of ascites is similar in both cirrhosis and CHF, we propose that a similar mechanism could cause bleeding into ascites in CHF.     

Learning needs of congestive heart failure patients

Congestive heart failure (CHF) affects approximately one-half million Canadians and five million Americans. Patient education is a vital component of nursing care of this population, with the goals of improving the CHF patient's quality of life, minimizing symptoms and hospital admissions, and reducing length of hospital stay. A review of the literature related to the educational needs of CHF patients reveals minimal research. The purpose of this study was to compare the perceived learning needs of CHF patients by patients and nurses, and to identify existing gaps between their perceptions. Fifty (50) CHF patients and 47 cardiac nurses were surveyed using a modified version of the CHF Patient Learning Needs Inventory developed by Hagenhoff et al. This instrument measured the importance of specific learning topics within the categories of anatomy and physiology, medications, diet, risk factors, activity, psychological factors, and other pertinent information. The results indicated that both groups found most information "moderately" to "very" important to learn. The patients generally rated all information items higher than nurses did. The most significant finding was that the nurses rated the diet category as second in importance, while the patients rated it last. The results from the study will be incorporated into a needs-based educational program for CHF patients.     

Calcium antagonists and sympathetic activity in congestive heart failure

OBJECTIVE: To review the sympathetic abnormalities occurring in heart failure, their pathophysiological importance and clinical relevance, and the effects of drug treatment, with particular reference to calcium antagonists. SYMPATHETIC ACTIVATION IN HEART FAILURE: Indirect and direct approaches to study sympathetic function in humans have documented conclusively that sympathetic activation represents a hallmark of cardiac failure syndrome. Evidence indicates that sympathetic overactivity is associated with, and probably caused by, a baroreflex impairment and that it has adverse effects on patients' prognosis and survival. GOALS OF DRUG TREATMENT IN CONGESTIVE HEART FAILURE: In the past, drug treatment in heart failure was aimed at improving patients' survival by ameliorating cardiac hemodynamics. It is now established that a major goal of therapeutic intervention is also to reduce sympathetic activation characterizing heart failure. CALCIUM ANTAGONISTS IN HEART FAILURE: Studies with short-acting calcium antagonists show that they enhance sympathetic activation and that this has an adverse effect on patients' survival. In contrast, third generation calcium antagonists such as amlodipine, which have a slow onset and long duration of action, do not adversely affect sympathetic function and reflex cardiovascular control. Indeed, evidence suggests calcium antagonists with this profile may exert favorable clinical effects.     

Exercise-related ventilatory abnormalities and survival in congestive heart failure

This retrospective study of 104 New York Heart Association class 1 to 4 heart failure patients undergoing exercise stress testing with gas exchange analysis demonstrated that the ventilatory equivalent for carbon dioxide at anaerobic threshold is useful in determining prognosis in patients with severe congestive heart failure, particularly when used in combination with peak exercise oxygen consumption. A ventilatory equivalent for carbon dioxide >50 and peak oxygen consumption < or =15.0 ml/kg/min defines a very high-risk patient group who should be prioritized for transplantation.     

Captopril and spironolactone therapy for refractory congestive heart failure

Short- and long-term clinical effects of the angiotensin-converting enzyme (ACE) inhibitor captopril in severe congestive heart failure (CHF) were evaluated during a 3-year open study of 124 inpatients with New York Heart Association (NYHA) functional class III or IV CHF refractory to treatment with cardiac glycosides and high doses of loop diuretics. Captopril was added to each patient's regimen, which comprised combinations of furosemide (124 patients), digitalis (117 patients), and spironolactone (90 patients). By the end of the first month of captopril administration, improvement in NYHA functional class was seen in 89 patients (72%). During the first year of captopril treatment, the number of hospital admissions and hospital days declined significantly (p < 0.001) and functional class improved significantly (p < 0.001). Although most patients tolerated captopril well, 44% experienced hypotension, which in 10% of patients necessitated termination of captopril therapy. Although mean serum potassium levels tended to increase, serious hyperkalemia did not occur. After 1 year, a subset of 30 patients who had not initially received spironolactone deteriorated clinically and manifested increasing urinary aldosterone levels. Hypotension precluded increasing the captopril dose, but introduction of spironolactone improved clinical status in this cohort. The results suggest that rational therapy for severe CHF includes addition of the aldosterone antagonist spironolactone to low doses of captopril (or another ACE inhibitor) and high doses of loop diuretics, provided renal function is adequate.     

Results of the ATLAS study. High or low doses of ACE inhibitors for heart failure?

In a large, randomized study, patients with heart failure who received a large daily dose of an angiotensin-converting inhibitor had a trend toward a lower mortality rate than did patients who received a low daily dose. Moreover, the hospitalization rate was lower in the high-dose group, and the side-effect profile was the same in both groups. Physicians should try to give maximal doses to achieve optimum benefit in this patient population.