Process management in hospitals: an empirically grounded maturity model

In order to improve transparency and stabilise health care costs, several countries have decided to reform their healthcare system on the basis of diagnosis-related groups (DRG). DRGs are not only used for classifying medical treatments, but also for case-based reimbursement, hence induce active competition among hospitals, forcing them to become more efficient and effective. In consequence, hospitals are investing considerably in process orientation and management. However, to date there is neither a consensus on what capabilities hospitals need to acquire for becoming process-oriented, nor a general agreement on the sequence of development stages they have to traverse. To this end, this study proposes an empirically grounded conceptualisation of process management capabilities and presents a staged capability maturity model algorithmically derived on the basis of empirical data from 129 acute somatic hospitals in Switzerland. The five capability maturity levels start with 'encouragement of process orientation' (level 1), 'case-by-case handling' (level 2), and 'defined processes' (level 3). Ultimately, hospitals can reach the levels 'occasional corrective action' (level 4) and 'closed loop improvement' (level 5). The empirically derived model reveals why existing, generic capability maturity models for process management are not applicable in the hospitals context: their comparatively high complexity on the one hand and their strong focus on topics like an adequate IT integration and process automation on the other make them inadequate for solving the problems felt in the hospital sector, which are primarily of cultural and structural nature. We deem the proposed capability maturity model capable to overcome these shortcomings

Rapidly progressive dyspnea in gastrointestinal stromal tumor (GIST) with imatinib cardiac toxicity

Gastrointestinal stromal tumors (GISTs) are rare and current estimates range from 4,000 to 6,000 number of GIST cases in the USA annually. Imatinib, a tyrosine kinase inhibitor, has shown a survival benefit in GISTs, and the presence of KIT mutation status is predictive of response. The current case discusses rapidly progressive dyspnea and heart failure in an elderly male with metastatic GIST who was started on imatinib. Although reported as a rare and sporadic side effect of imatinib, the current case illustrates rapidity and the clinical significance of cardiotoxicity, with onset at 2 weeks. Cases of imatinib-induced cardiotoxicity can range from being mild ventricular dysfunction to overt heart failure. Prior to starting imatinib, our patient had a history of hypertension. He subsequently ended up developing heart failure as acknowledged by the echocardiogram (ECHO). In general, elderly with preexisting cardiovascular comorbidity are at greater risk. The goal in such situations is immediate discontinuation or reduction of the imatinib dosage. The case prompts for awareness of imatinib cardiotoxicity. Moreover, a pretreatment cardiac assessment along with monitoring throughout therapy is therefore advisable. Also, imatinib-induced cardiotoxicity should be differentiated from imatinib-associated fluid retention, in which ECHO findings can be normal. This case report raises the concern for accelerated cardiotoxicity profile of imatinib. Further prospective studies with multidisciplinary input are needed to establish this association further

Traumatic intracranial hemorrhage correlates with preinjury brain atrophy, but not with antithrombotic agent use: a retrospective study.

The impact of antithrombotic agents (warfarin, clopidogrel, ASA) on traumatic brain injury outcomes is highly controversial. Although cerebral atrophy is speculated as a risk for acute intracranial hemorrhage, there is no objective literature evidence.This is a retrospective, consecutive investigation of patients with signs of external head trauma and age ≥60 years. Outcomes were correlated with antithrombotic-agent status, coagulation test results, admission neurologic function, and CT-based cerebral atrophy dimensions.Of 198 consecutive patients, 36% were antithrombotic-negative and 64% antithrombotic-positive. ASA patients had higher arachidonic acid inhibition (p = 0.04) and warfarin patients had higher INR (p<0.001), compared to antithrombotic-negative patients. Antithrombotic-positive intracranial hemorrhage rate (38.9%) was similar to the antithrombotic-negative rate (31.9%; p = 0.3285). Coagulopathy was not present on the ten standard coagulation, thromboelastography, and platelet mapping tests with intracranial hemorrhage and results were similar to those without hemorrhage (p≥0.1354). Hemorrhagic-neurologic complication (intracranial hemorrhage progression, need for craniotomy, neurologic deterioration, or death) rates were similar for antithrombotic-negative (6.9%) and antithrombotic-positive (8.7%; p = 0.6574) patients. The hemorrhagic-neurologic complication rate was increased when admission major neurologic dysfunction was present (63.2% versus 2.2%; RR = 28.3; p<0.001). Age correlated inversely with brain parenchymal width (p<0.001) and positively with lateral ventricular width (p = 0.047) and cortical atrophy (p<0.001). Intracranial hemorrhage correlated with cortical atrophy (p<0.001) and ventricular width (p<0.001).Intracranial hemorrhage is not associated with antithrombotic agent use. Intracranial hemorrhage patients have no demonstrable coagulopathy. The association of preinjury brain atrophy with acute intracranial hemorrhage is a novel finding. Contrary to antithrombotic agent status, admission neurologic abnormality is a predictor of adverse post-admission outcomes. Study findings indicate that effective hemostasis is maintained with antithrombotic therapy

Patient Traits and Outcomes.

<p>Patient Traits and Outcomes.</p

Pre-existing Medical Conditions by Antithrombotic Status.

<p>Pre-existing Medical Conditions by Antithrombotic Status.</p

Injury Severity Score and AIS Values by Antithrombotic Status.

<p>AIS, Abbreviated Injury Scale score; AT, antithrombotic.</p><p>Injury Severity Score and AIS Values by Antithrombotic Status.</p

Head Trauma ICH Risk Conditions by Antithrombotic Status.

<p>ICH, intracranial hemorrhage; AT, antithrombotic.</p><p>Head Trauma ICH Risk Conditions by Antithrombotic Status.</p

Outcomes According to Antithrombotic and Admission Major Neurologic Dysfunction Status.

<p>AT, antithrombotic; (−), negative; (+), positive; AMND, Admission Major Neurologic Dysfunction; ICH, intracranial hemorrhage; AIS, Abbreviated Injury Scale score.</p><p>Outcomes According to Antithrombotic and Admission Major Neurologic Dysfunction Status.</p