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[Low-molecular-weight heparin without oral anticoagulants for the treatment of deep vein thrombosis]. / Tratamiento de la trombosis venosa profunda con heparinas de bajo peso molecular. Estudio comparativo con anticoagulación oral.

BACKGROUND AND METHODS: The available data on the utility of low-molecular-weight heparins (LMWH) in the secondary prophylaxis of deep vein thrombosis (DVT) are limited. We compared two cohorts of patients diagnosed of DVT. One group followed treatment with LMWH and the other group did with oral anticoagulants (acenocoumarol). Safety was evaluated by the rate of major hemorrhage and 2.5-years period fracture rate, and efficacy was evaluated as the rate of early recurrence and one-year recurrence rate. RESULTS: Of 65 patients treated with LMWH, the hemorrhagic rate was 1.5% (95% CI 0.08-9.40), fracture rate was 7.7% (95% CI 2.87-17.75), early recurrence was 1.5% (95% CI 0.08-9.40) and one-year recurrence was 3% (95% CI 53-11.64). In 118 patients treated with oral anticoagulants the hemorrhagic rate was 3.4% (95% CI 1.09-8.97), odds ratio 0.33, the fracture rate was 11% (95% CI 16.23-18.44), odds ratio 0.66, the early recurrence rate was 5% (95% CI 2.08-11.20), odds ratio 0.60 and one-year recurrence was 3.4% (95%CI 1.09-8.97), odds ratio 0.33. CONCLUSIONS: Secondary prophylaxis of DVT with LMWH is as safe and effective as classical treatment with oral anticoagulants. In this study the 2.5-year period fracture rate was similar in both groups of treatment.

[Cardiac tamponade caused by hydatid pericarditis]. / Taponamiento cardiaco por quiste hidatídico pericárdico.

We present the case of a woman with no previous clinical history of disease, that debuted with acute heart failure with symptoms of cardiac tamponade from hydatic pericarditis as a result of a fistula across the diaphragm secondary to a hydatidic cyst rupture in the liver. Cardiac hydatidosis is rare with an incidence in some series between 0.2-2% in humans infested with Echinococcus, affectation of the pericardia being rare. For this reason we present a revision of its pathogenesis, clinical presentation, diagnosis and recommended treatment.

[Acute lung embolism: a prospective study from May 1992, to May 2002]. / Embolismo pulmonar agudo. Un registro de 10 años: de mayo de 1992 a mayo de 2002.

INTRODUCTION: To define de prevalence, the clinical profile, the predisposing factors and the hospital evolution of clinical acute lung thromboembolism episodes. MATERIAL AND METHODS: A prospective study from May 1992, to May 2002, of acute lung embolism in an Internal Medicine ward with 8 beds in Hospital of Navarra (EPHONA). Clinical acute lung thromboembolism is defined by the clinical characteristics together the demonstration of thrombi in the lung arteries with arteriography, helicoid computerized axial tomography, or high or average probability lung gammagraphy, together the demonstration of deep venous thrombosis with doppler ultrasound or phlebography. We compared the clinical spectrum with that of international clinical series, evaluated the possibility of clinical syndromes according to the size of the affected vessel (central vs. peripheral), and compared the characteristics of patients with manifest deep venous thrombosis with those of the patients with clinical acute lung thromboembolism and without a known emboli source. RESULTS: In the period of 10 years, and with 2,493 patients admitted, 106 clinical acute lung thromboembolism were diagnosed (prevalence: 4.25%; CI: 3.51-5.14; p < 0.05); these patients were 72 +/- 11 years, in other words, an age 5 years higher than the rest of the patients (p < 0.001). There was a delay of 10 days from the beginning of the symptomatology up to the hospitalization. The clinical spectrum was similar to that of other reported series except by the presence of cough and pleural rub (p < 0.001). The main predisposing factors were immobility (41%) and cancer (25%). Hospital mortality was 3.77%. In 70 (66%) patients we obtained information on the affected vessel, not being fulfilled the association of specific clinical syndromes with the size of the vessel, although the patients with central clinical acute lung thromboembolism showed higher deterioration of gas exchange (p = 0.002) and higher activation of the fibrinolysis (p = 0.012) than patients with peripheral clinical acute lung thromboembolism. 35% of episodes of clinical acute lung thromboembolism developed without simultaneous deep venous thrombosis and showed higher disturbance of gas exchange (p = 0.03) and arterial hypotension (p = 0.02). CONCLUSIONS: Clinical acute lung thromboembolism is a frequent condition that occurs in patients of advanced age and that shows low hospital mortality when is diagnosed and treated even with a 10-day delay up to the diagnosis. The clinical spectrum is similar to that observed in other parts of the world, but the cough as a prominent a symptom and the pleural rub should propose other diagnostic alternatives. The size of the affected pulmonary vessel is not related with a specific clinical syndrome, although the central clinical acute lung thromboembolism evolves with higher disturbance of the gas exchange. In the third of clinical acute lung thromboembolism episodes an emboli source is not demonstrated, perhaps because all emboli has migrate to the pulmonary arteries; these episodes give rise to higher hypotension and disturbance of the gas exchange.

[Eight cases of rheumatism associated with cancer]. / Ocho casos de reumatismos asociados a cáncer.

OBJECTIVE: To study the rheumatic diseases associated with cancer diagnosed in an Internal Medicine Service. MATERIAL AND METHODS: A retrospective and descriptive study of the patients diagnosed during 1992-2000 of different rheumatic diseases associated with cancer. RESULTS: During a period of 9 years we identified 8 cases of paraneoplastic rheumatisms about a total of 2,127 patient, representing an incidence of 3.7@1000, with a predominance in males. The consultation motive in all them was the clinic of the rheumatic disease. Six of the eight neoplasias were adenocarcinomas. CONCLUSIONS: Though the paraneoplastic rheumatisms are not frequent, it is necessary take into account their existence when exist antecedent of neoplasia, in patient male and when the clinical course or response to the treatment is atypical.

[Pulmonary thromboembolism: long term course and clinical epidemiology]. / Tromboembolismo pulmonar: evolución a largo plazo y epidemiología clínica.

BACKGROUND: Long-term clinical course of pulmonary thromboembolism is not well-known. Our aim was to know the events which occur to in-patients diagnosed of pulmonary embolism. METHODS AND PATIENTS: This is a prospective observational study from May-92 to December-2002 with all in-patients diagnosed of pulmonary thromboembolism at a clinical area of Internal Medicine. Main targets were to know survival, relapses, major hemorrhage rate (Defined as those episodes of bleeding which needed blood transfusion and readmission) and cancer associated rate (Previous and newly diagnosed cancer). Follow up were carried out with telephone contacts with patients and relatives in case of death, and with the computerized system of patients and clinical events of Health Service of Navarra. RESULTS: One hundred and sixteen patients were included in the study (Mean age 72 SD 11 years male 54%). During index episode 4 (3.7%) patients dead. Ten patients were lost in follow up. The rest 102 patients were traced for 31.81 SD 31.23 months (Range 1-127). Relapse rate was 19.6% that occurred 22.64 SD 24.57 (Range 1-73) months after index episode (Twelve pulmonary embolisms, 5 deep venous thromboses and 3 sudden death with dyspnea). Major hemorrhage rate was 10.4%. During follow up 14 (13.7%) new cancers were diagnosed (Lung 4, prostate 2, bladder 2, and colorectal, ovary, breast, liver and kidney one each one). At all prevalence of cancer associated with pulmonary thromboembolism was 31%. Mortality rate was 37% (Men 25%, women 49%, p < 0.01). Main causes of death were cancer (32%) and relapse of pulmonary thromboembolism when joined with treatment complications 24%. Half of deaths occurred in the first year of follow up, showing a shortened survival those patients with cancer (p = 0.02) and patients with relapses of pulmonary embolism (p = 0.06). Beyond the first year, mortality declines to a rate of 10% per year mainly because of cardiovascular causes. Mortality associated factors were age > 75 years (p < 0.001) gender female (p < 0.01), a delayed admission and treatment from the beginning of symptoms (p < 0.05), higher LDH level (p < 0.01) and coexistence of cancer (p < 0.05). In logistic-regression analysis age, delayed admission and treatment and higher LDH levels were predictors of long-term death. CONCLUSIONS: Patients with pulmonary embolism show a high mortality rate, with a critical period during the first year after index episode, being deaths associated to cancer and to a composite of relapse of venous thromboembolic disease and bleeding complications. Mortality rate beyond the first year declines, being deaths explained because of cardiovascular causes. An advanced age, a delayed diagnosis and treatment and serum LDH may predict long-term mortality.

C-reactive protein as a predictor of improvement and readmission in heart failure.

OBJECTIVES: Only recently, new risk factors to explain atherosclerotic disease have been identified. One of the most important clinical manifestations of atherosclerosis is heart failure. Our study was aimed at investigating C-reactive protein (CRP), a marker of systemic inflammation, in the context of heart failure, and to determine its usefulness in predicting the need for readmission in patients with heart failure and their degree of improvement. DESIGN: We studied patients admitted to our hospital due to heart failure, independent of the cause. CRP levels were measured with a sensitive standard assay on a Nephelometer analyser. Patients were classified on admission and discharge following New York Heart Association (NYHA) functional criteria; left ejection fraction was also determined by transthoracic echocardiography. Patients presenting clear sources of infection or inflammatory disease were excluded. Our control group consisted of patients admitted for syncope. Each patient was followed up through a computer system controlling admissions to and discharge from the hospital, for a period of 18 months after initial admission. End points considered were NYHA functional class on discharge, readmission and death. RESULTS: We studied prospectively 76 patients with a mean age of 73.5+/-11 [95% confidence interval (CI) 71.2-75.8]; 44 were male (58%) and 32 female (42%). The mean CRP level in patients with heart failure was 3.94+/-5.87 (95% CI, 1.26-7.60), while in 15 patients with syncope it was 0.84+/-1.95 (95% CI, 0.96-2.94) (P=0.0007). The principal causes of heart failure included dilated cardiomyopathy due to coronary arterial disease (30%), valvular disease (28%) and heart failure secondary to hypertension (25%). The mean left ejection fraction adequately measured in 72 (95%) patients was 50.41+/-9.88 (95% CI, 41.20-59.65). We observed a trend of higher CRP levels in relation to ejection fractions below 35%: 7.50+/-9.88 vs. 3.75+/-4.57, (P=0.09). Our results showed that on discharge CRP levels increased in relation to NYHA class: I: 0.74+/-0.69; II: 3.78+/-3.76; III: 7.4+/-8.65; IV: 12.2+/-15.27 (P<0.05). On follow-up of each patient for 18 months, 32 (43%) were readmitted due to deterioration of their heart condition. For patients who were readmitted, those presenting CRP levels >0.9 mg/dl were identified as candidates for earlier hospitalisation than those with levels below 0.9 mg/dl (P=0.02) RR=1.43. In logistic-regression analysis the only group of tested variables predicting readmission were levels of CRP, NYHA class and plasmatic K on discharge and left ventricle ejection fraction. Analysis of covariates yields CRP levels as being an independent predictor of readmission. CONCLUSIONS: An inflammatory response is present in deteriorating heart failure. We observed higher CRP levels in patients with higher NYHA functional class, perhaps signalling a poor therapeutic response. Higher CRP levels were also related to higher rates of readmission and mortality and it could be an independent marker of improvement and readmission in heart failure.

[Hospital readmission in internal medicine]. / Reingreso hospitalario en Medicina Interna.

BACKGROUND: The readmission rate could be a valuable tool as measurement of hospital quality. Readmissions are due to several factors: clinical, hospital related and patient related. We analyze readmission to internal medicine in a hospital of third level. MATERIAL AND METHODS: During 11 months in 1988 we counted all readmissions (R) defined as every previous admission occurred in a span of five years into an area of internal medicine composed by 8 beds. We counted number of readmssions, time from the last readmission, living area (city vs country), sort of primary care physician (GP vs family care specialist), living way (single, with family, institution, homeless). Precipitating factors were observed as well as diseases causing it. R were classified as R related (RR) when readmission was provoked by the same pathological condition or a complication. Multi-readmission (MR), those R caused by the same disease process and treated in different areas and services of the hospital. Avoidable R (AR), those R which did not fullfil AEP criteria. Early readmission (ER) those R occurring before 30 days after last discharge. RESULTS: Three hundred and eleven patients (mean age 67.93 (SD 15.51), males 64%, mean length of stay 7.75 (SD 4.35), 93% admitted from emergency yard, mortality rate 3.5%) were included. R were 111 (35.5%), RR 83 (26 and 75% of RR), MR 68 (82% of RR), ER 33 (39.7% of RR) and AR 16 (19.2% of RR) patients. The most frequent diseases were heart failure and chronic respiratory diseases. Main causes of R were worsening of chronic disease 41 (37%), non-appropriale ambulatory management 24 (22%) erroneous diagnosis 8 (7%), iatrogenic effect 7 (6%), new disease 29 (26%) and others 2 (2%). Mortality rate in R patients was 7.2% (confidence interval 95% 2 to 9%). Number of readmissions were 3.22 (SD 2.25) and time to readmission 8.99 (SD 11.96) months. Living in city (p < 0.05) and to be cared by family physician (p < 0.01) both were factors accelerating readmission. Patients with RR had a higher number of readmissions (3.55 SD 2.23 p < 0.001) and they occurred sooner (8.03 SD 11.85) (p < 0.01). There was a trend to higher readmission rate in female (p 0.052). Fifty-seven percent of RR patients did not have consultation with primary care physician (p < 0.05) (confidence interval 95% 3 to 39%). Consultation with primary care yielded a delay in readmission of 5 months (p < 0.01). Patients with MR had an increased number of readmissions (p < 0.01). Associated factors were iatrogenic effect (p < 0.05), non-appropriate ambulatory management (p < 0.001) and worsening chronic disease (p < 0.001). Patients with ER were readmitted 0.45 (SD 0.30) months after the last discharge and they had a higher mortality rate (p < 0.05). Patients with AR had a mean length of stay shorter (p < 0.05), a trend to higher readmission rate (p = 0.06) and sooner (p = 0.08) with a null mortality rate (p < 0.01). As risk factors for RR in logistic regression were identified MR, AR, ER and causes of readmission consisting in worsening of chronic disease, non-appropriate ambulatory management, erroneous diagnosis and iatrogenic effect. CONCLUSIONS: Our readmission rate is 26%, chronic respiratory diseases and heart failure being the main diseases. Over 39% of causes of readmission could be preventable and there is a facilitation phenomenon in number and time to readmission caused by previous readmissions. Risk factors for readmission in internal medicine are multi-readmission, early and avoidable readmission and as specific causes worsening of chronic disease, non-appropriate ambulatory management, erroneous diagnosis and iatrogenic effect.

[ACTH-independent Cushing's syndrome due to bilateral macronodular adrenal hyperplasia with empty sella turcica and anterior panhypopituitarism]. / Síndrome de Cushing ACTH-independiente por hiperplasia adrenal macronodular bilateral con silla turca vacía y panhipopituitarismo anterior.

A case is presented of Cushing's syndrome due to macronodular bilateral adrenal hyperplasia which is ACTH-independent as was demonstrated by the undetectable basal and after stimulation with metoprolol ACTH plasma levels. High cortisol levels is associated in this patient with empty sella turcica and anterior panhypopituitarism with confirm the exclusive adrenal origin of the hormone hypersecretion and the lack of treatment success with hypophysis ablation in this process.