Alleged malpractice in orthopaedics. Analysis of a series of medmal insurance claims.

BACKGROUND: Medical malpractice is an important topic worldwide, and orthopedics is a clinical branch that is considered to be at a high risk for claims. The analysis of a series of medmal insurance claims allows forensic pathologists, clinicians, and insurance companies to probe the risk of a specific clinical branch for medical malpractice claims and highlights areas where care may be improved. We investigated the main features of a major Italian insurance broker's archive in order to identify recurrent pitfalls in this field. MATERIALS AND METHODS: A retrospective study was carried out on orthopedics claims. The archive covered claims from 2002 to 2013 that targeted 1980 orthopedists. RESULTS: 635 claims were found and analyzed with a focus on the clinical activity invocked in the claim, the presence of alleged team malpractice, the clinical outcome of the case, and the final forensic decision regarding the claim. 299 orthopedists had at least one malpractice claim made against them during the available period; 146 orthopedists were subject to more than one malpractice claim. Most of the claims regarded perioperative and operative cases, usually originating from civil litigation. The anatomical sites most commonly involved were the hip or knees, and sciatic nerve lesions were the main contributor. CONCLUSIONS: Orthopedics is a medical specialty with a high risk for malpractice claims. In our study, medical malpractice was observed in nearly 50% of the cases-typically in surgery-linked cases resulting in permanent impairment of the patient. Death from orthopedics malpractice seemed to be rare. LEVEL OF EVIDENCE: IV.

KIF3C, a novel member of the kinesin superfamily: sequence, expression, and mapping to human chromosome 2 at 2p23.

Kinesins are microtubule-dependent molecular motors involved in intracellular transport and mitosis. Here, we report the cloning, sequencing, mapping, and expression of a novel member of the kinesin superfamily. The sequence of this newly identified human cDNA reveals an open reading frame encoding a putative protein of 792 residues. Based on its high sequence similarity to the kinesin-like molecule KIF3B, we named this protein KIF3C. KIF3C is encoded by transcripts that are distinct from the KIF3B mRNA in human, rat, and mouse and is preferentially expressed in the brain. Fluorescence in situ hybridization reveals that, in the human genome, the KIF3C gene maps to chromosome 2 at 2p23. The sequence of KIF3C predicts an unusually long insertion in the proximity of L11, a region thought to mediate microtubule binding. Taken together, these findings suggest that KIF3C is a novel kinesin-like protein that might be specifically involved in microtubule-based transport in neuronal cells.

Expression of neuronal kinesin heavy chain is developmentally regulated in the central nervous system of the rat.

The kinesin family of motor proteins comprises at least two isoforms of conventional kinesin encoded by different genes: ubiquitous kinesin, expressed in all cells and tissues, and neuronal kinesin, expressed exclusively in neuronal cells. In the present study, we have analyzed the expression of the two kinesin isoforms by immunochemistry at different stages of development of the rat CNS. We have found that the level of expression of neuronal kinesin is five to eight times higher in developing than in adult rat brains, whereas that of ubiquitous kinesin is only approximately 2.5 times higher in maturing versus adult brains. Moreover, we have studied the distribution of neuronal kinesin by light microscopic immunocytochemistry in the rat brain at different postnatal ages and have found this protein not only to be more highly expressed in juvenile than in adult rat brains but also to show a different pattern of distribution. In particular, tracts of axonal fibers were clearly stained at early postnatal stages of development but were markedly unlabeled in adult rat brains. Our results indicate that the expression of at least one isoform of conventional neuron-specific kinesin is up-regulated in the developing rat CNS and suggest that this protein might play an important role in microtubule-based transport during the maturation of neuronal cells in vivo.

Differential expression of ubiquitous and neuronal kinesin heavy chains during differentiation of human neuroblastoma and PC12 cells.

Kinesin is a microtubule-based motor protein involved in intracellular organelle transport. Neurons are characterized by the presence of at least two isoforms of conventional kinesin: ubiquitous kinesin, expressed in all cells and tissues, and neuronal kinesin, whose pattern of expression is confined to neuronal cells. In order to investigate whether the two kinesin motors, which are encoded by different genes, may play distinct biological roles in neurons, we studied their expression during neuronal differentiation. Human neuroblastoma SH-SY5Y and IMR32 cells and rat phaeochromocytoma PC12 cells were used as an in vitro system for neuronal differentiation and were induced to differentiate in the presence of retinoic acid, a combination of dibutyryl cAMP and 5-bromodeoxyuridine, and nerve growth factor respectively. The expression level of each kinesin isoform was evaluated by quantitative immunoblot before and after pharmacological treatment. We found that in all cell types the expression level of neuronal kinesin, but not of ubiquitous kinesin, is stimulated during differentiation. In particular, SH-SY5Y cells show a 4.5-fold, IMR32 cells a 3-fold and PC12 cells a 7-fold increase in the level of expression of neuronal kinesin. By Northern blot analysis we found that the selective increase in the expression of neuronal kinesin is paralleled by an increase in its mRNA, indicating that there is a transcriptional control of the expression of this kinesin isoform during differentiation of neuroblastoma and PC12 cells. Our results suggest that these cells represent an adequate model to study the function of conventional kinesin and its isoforms.

[Neuroleptic malignant syndrome. A case report]. / Sindrome maligna da neurolettici. Caso clinico.

A lethal case of neuroleptic malignant syndrome in a 42-year-old woman with a history of bipolar psychiatric disorder under treatment with haloperidol is reported. The patient, hospitalized many times in the past for psychiatric treatment, was then admitted for treatment of a relapse of the disease during a exceedingly hot period. The patient complained of hallucinations and stomach ache. It was necessary to increase the dose of haloperidol to 2 mg, 3 times a day, and to give a single dose of perphenazine enanthate 100 mg. All tests proved normal except for CPK 274 U/l and urea 14 mg/dl. On hospital day 2, went into coma with high temperature, diaphoresis, polyuria, leucocytosis (WBC count 15,440 U/mm3), urea 7 mg/dl, LDH 425 U/l, Na 114 mEq/l, K 2.5 mEq/l. The rapid improvement following hypertonic saline treatment encouraged a diagnosis of water intoxication. On hospital day 7, continuing with the haloperidol treatment, the patient developed a high temperature and deterioration torpor. On hospital day 9, the patient went back into coma with temperature over 40 degrees C (104 degrees F), with fine myoclonia most visible on the face, and muscular rigidity. The CPK, rose from 5,169 to 28,060 U/l in less than 24 hours; the serum myoglobin rose to 41,000 ug/l. On day hospital 11 developed renal, cardiac and respiratory insufficiency. The picture deteriorated and dantrolene was no longer of use in controlling the fever. Then with a fever of over 42 degrees (108 degrees F) and the CPK at 50,000 the patient died. The autopsy demonstrated widespread rhabdomyolysis, a picture of widespread aspecific shock in all organs and picture of myoglobin-induced tabular necrosis of the kidney.

The metabolic processing of glycosphingolipids in HT-29 cells is differentiation-dependent.

The metabolism of two radiolabelled glycosphingolipids, lactosylceramide and GM1 ganglioside, in differentiated and undifferentiated HT-29 cells is reported. Both lactosylceramide and GM1 ganglioside were demonstrated to be extensively catabolized in undifferentiated cells, as deduced by the relative amount of the compounds formed along the degradative pathway. Conversely, in differentiated cells both precursors were utilized as substrates for sugar-chain elongation. Furthermore we were unable to detect any significant difference in the activity of CMP-NeuAc:GM1 alpha 2-->3 sialyltransferase, a Golgi key enzyme for the glycosylation of glycosphingolipids, between the two cell populations. Taken together with our previous results on the differentiation-dependent trimming of high-mannose N-linked glycoproteins in HT-29 cells, one can suggest that common steps control the anabolic/catabolic balance of these two classes of glycoconjugates as a function of differentiation.

[The estimation of p50 by the algorithm proposed by Siggard-Andersen. Its experimental assessment in critical patients]. / Calcolo della p50 mediante l'algoritmo proposto da Siggaard-Andersen. Valutazione sperimentale in pazienti critici.

STUDY OBJECTIVE: To determine the ability of O. Siggaard-Andersen algorithm in the estimation of the "in vivo" p50 and standard p50 values from a single blood sample with sO2% less than or equal to 97. DESIGN: comparison between measured and calculated standard p50 values. SETTING: Intensive care unit. PATIENTS: thirteen cardio-pulmonary critical ill patients. Mean age of seventy-four years (range 53-84 years). MEASUREMENT: The experimental measurement of p50 standard (p50st sper) was performed tonometering the venous blood samples (60 specimens) using an IL-237 tonometer at 37 degrees C, with two different gas mixtures to obtain pCO2 at 5.33 kPa (DS = 0.06), and pO2 at levels to achieve sO2% values close to 50%. The gases's complete equilibration was not deemed important. The pO2 values were corrected to a pH of 7.40 using a Bohr factor = -0.48 and the p50 was taken by simple interpolation of points on the sO2%/pO2 diagram. Calculated standard p50 (p50st calc) and calculated "in vivo" p50 on the venous specimens (No. 60) and the correspondent arterial specimens with sO2% less than or equal to 97 (No. 40) were obtained by Siggaard-Andersen's computerized algorithm. Blood specimen analysis was performed by means of an ABL3 Radiometer gas analyzer and an OSM3 Radiometer oximeter. Statistical analysis was made by Anova test for liner regression. RESULTS: There was excellent correlation between the 60 experimental p50st determined by Siggaard-Andersen's oxygen dissociation curve on the same blood samples. The regression equation was: p50st sper = -0.79 + 1.21 x p50st calc, r = 0.90, R2 = 81.1%; with F = 249.5 and less than 10(-5). No good correlation was found between p50st and standards p50 calculated on arterial specimens (p50st calc art): p50 = 1.38 + 0.52 x p50st calc art, r = 0.52, R2 = 26.6%, F = 14 e P less than 10(-3). Regression of in vivo P50 calculated on correspondent venous samples (p50 ven) was: p50 ven = 0.79 = 0.77 x p50 art, r = 0.93, R2 = 87.2%, F = 256 and P less than 10(-5). CONCLUSION: Our results suggest that the curve describes the curve also at high saturation when it is not longer linear. Accurate measurement (including dishemoglobin percentage) and sO2% less than or equal to 97 are necessary. We did not perform experimental measurements of "in vivo" p50 but we postulate that as the p50st was well calculated so too would be the p50 "in vivo" at 37 degrees C.

[Hypoxia and oxygen content during dialysis]. / Ipossia e contenuto di ossigeno durante dialisi.

In a study of 72 patients treated with acetate and bicarbonate dialysis, the Authors verified if hypoxic hypoxia caused by dialysis depends on a deficit in oxygen content with an inherent risk of tissue hypoxia. PO2uv (uncompensated venous oxygen partial pressure) and CQ (cardiac compensation factor) derived from the oxygen absorption curve were studied by a new Ole Siggard-Andersen algorithm. The results do not show a risk of tissue hypoxia in the postdialytic period.

[Clonidine abstinence syndrome. A clinical case]. / Sindrome da astinenza da clonidina. Caso clinico.

During hospitalization a patient with acute pulmonary oedema caused by myocardial dilation and chronic kidney failure presented high blood pressure and repeated episodes of supraventricular tachycardia. The complication was attributed to the withdrawal of clonidine and was treated by reintroduction of the drug combined with nifedipine, nitroderivates and antiarrhythmic drugs.

[ARDS in MOFS (multiple organ failure syndrome). How to direct the therapy? A case report of MOFS in AIDS]. / ARDS componente della MOFS (multiple organs failure syndrome) come orientare la terapia? Descrizione di MOFS in AIDS.

A young AIDS patient was admitted to the Intensive Therapy ward of our hospital with ARDS. The case raised the question of how medical and nursing personnel should face the problem of "suitable treatment for a terminally ill patient". Therapy was based on invasive methods such as mechanical ventilation and the insertion of catheters to monitor vital parameters. The evolution of ARDS in MOFS revealed the difficulty of sustaining vital parameters and avoiding pluriorganic damage.

The oxygen status of the arterial blood in the critically ill.

In Critical Care medicine the concepts of Oxygen Delivery, Oxygen Consumption and Tissue Oxygenation have become fundamental in clinical practice but measurements of Oxygen Content and O2 Transport variables require invasive procedures that could be dangerous for critically ill patients and trigger a septic process. Derived indices obtained combining data from a Blood Gas Analyzer with the data from a multi-wavelength spectrophotometer and using the Ole Siggaard-Andersen pH/Blood Gas computerised algorithm might be the non-invasive answer. On 115 arterial blood samples from critically ill patients, we measured pH, pCO2, pO2, oxygen saturation, total hemoglobin concentration and fractions of carboxy- and methemoglobin. The new algorithm was used to calculate: active hemoglobin concentration, total oxygen concentration, actual half-saturation tension, 2,3-diphosphoglycerate concentration, estimated functional shunt, uncompensated mixed venous pO2 (assuming an arterio-venous oxygen difference of 2.3 mmol/L based on a standard oxygen consumption of 11.2 mmol/min and a standard cardiac output of 4.9 L/min) and the cardiac oxygen compensation factor. In Intensive Care all the oxygen parameters may be determined with sufficient accuracy and precision provided the oxygen saturation level is less than 0.97 and provided the definition of oxygen saturation is properly settled and measurements are performed according to the highest state of the art. However, in critically ill patients in evolution our aim is to maintain an 'optimal' paO2 on the plateau of the Oxygen Dissociation Curve (ODC) and the use of mechanical ventilation, high FIO2, fluid challenges and the rapid improvement of the patient's conditions can cause a value for sO2 greater than or less than 0.97 and an improvement or worsening of the paO2. The p50 calculation both in simultaneously drawn arterial and venous blood permits utilisation of derived indices (pO2uv-, CQ) for sO2 greater than 0.97. The Ole Siggaard-Andersen algorithm seems to give correct p50 values, at high saturation values, particularly when discarding unrealistic values for calculated cDPG. The correlation between p50 calculated by the Ole Sigaard-Andersen algorithm with that derived from classical formula shows the superiority of the findings obtained by means of the new algorithm. In critically ill patients the ODC is usually shifted to the right. The new parameters, pO2uv- and CQ, contain useful informations for clinical practise; but rapid changes in Cardiac Index (CI) and VO2/m2 can be ignored by the new algorithm, if these changes are not associated with a rise in ctO2 or pH and pCO2 changes.(ABSTRACT TRUNCATED AT 400 WORDS)

[Multiple organ failure syndrome in infection caused by ictero-hemorragic Leptospira. Description of a clinical case]. / MOFS (multiple organs failure syndrome) in corso di infezione da Leptospira ittero-emorragica. Descrizione di un caso clinico.

A 53 years old fisherman was admitted to General Intensive Care Unit in Arezzo with signs and symptoms of Weil disease. An early acute respiratory failure developed. Radiological and haemodynamic findings confirmed a diagnosis of ARDS. The patient developed a severe jaundice, acute renal failure and ARDS (MOF multiple organs failure). To support different failures of the organs, CMV (continuous mandatory ventilation: CPPV with PEEP max 10 cm H2; IRV max 2:1) and AMV (assisted mandatory ventilation: Pressure Support Ventilation), haemofiltration, haemoperfusion and plasmapheresis were simultaneously used, that got better and better renal and respiratory performances. Haemodynamic worsening by PEEP during extracorporeal treatment was overcome by PSV very useful new ventilatory procedure even during weaning period. The patient treated in such manner survived without important disabilities. This care confirms that ARDS (non cardiogenic edema) and MOF can develop during Icterohaemorrhagic Leptospirosis.