Quality improvements in end of life care: insights from two collaboratives.

BACKGROUND: Just a few generations ago, most people died suddenly, at any age. Now, most die of serious chronic disease, after a substantial period of disability. The care system does not serve this burgeoning population well. However, two quality improvement (QI) collaboratives sponsored by the Institute for Healthcare Improvement and the Center to Improve Care of the Dying set about making substantial improvements. INSIGHTS GAINED: The participating organization teams in two Breakthrough Series collaboratives found it best to identify patients by asking "Would it be surprising for this patient to die in the next year? (or the next few months?)" All the teams used standard QI approaches, with an aim, measures, and changes to try in Plan-Do-Study-Act cycles. In the first collaborative, 42 (89%) of the 47 teams made important improvements in their care systems. Because of the strength of their changes, the high performance of their team, the administrative support they received, and their ability to partner with other agencies, 13 (27%) of the teams made substantial, measurable improvement during the collaborative. In the second collaborative, 29 (85%) of the 34 teams made key changes to their care system, and 16 (47%) of the teams made substantial, measurable improvement. Coordination across programs such as between a hospital and a long term care facility or hospice remained an elusive goal, and good care cannot become routine without financing and coverage reform. CONCLUSION: Clinical providers can reliably make substantial improvements in end of life care, within a few months, and within current financing and regulation. Coordinated efforts in two Breakthrough Series produced generalizable insights.

Autonomic instability and hypertension resulting in subarachnoid haemorrhage in the Guillain-Barré syndrome.

We report the case of a 47-year-old woman with Guillain-Barré syndrome who developed autonomic instability and hypertension and subsequently developed a subarachnoid haemorrhage. This was manifested clinically by a seizure which began focally and became generalised. Computer tomography demonstrated a localised haemorrhage in the left central sulcus. Control of the hypertension was achieved with intravenous labetolol. Autonomic instability and hypertension are frequently reported in Guillain-Barré syndrome. Subarachnoid haemorrhage is an uncommon but serious complication.

Myoblast city, the Drosophila homolog of DOCK180/CED-5, is required in a Rac signaling pathway utilized for multiple developmental processes.

The Rac and Cdc42 GTPases share several regulators and effectors, yet perform distinct biological functions. The factors determining such specificity in vivo have not been identified. In a mutational screen in Drosophila to identify Rac-specific signaling components, we isolated 11 alleles of myoblast city (mbc). mbc mutant embryos exhibit defects in dorsal closure, myogenesis, and neural development. DOCK180, the mammalian homolog of Mbc, associates with Rac, but not Cdc42, in a nucleotide-independent manner. These results suggest that Mbc is a specific upstream regulator of Rac activity that mediates several morphogenetic processes in Drosophila embryogenesis.

A fax-back oxygenator-perfusionist clinical performance data collection and statistical analysis method.

A method to collect clinical oxygenator performance data daily is described. At the end of a bypass procedure, the perfusionist fills in a fax-back form designed to automatically input patient-oxygenator performance data into a computer spreadsheet. Multiple blood gases, FiO2, gas and blood flow data, venous oxygenator blood inlet conditions (hemoglobin, O2 saturation, hematocrit and temperature), time on bypass and device manufacturer information are collected at the end of each cardiopulmonary bypass procedure at multiple institutions. A large sample database is created that allows multi-parametric analyses in regard to clinical practice, device performance, manufacturing consistency and patient requirements. The database and analyses facilitate institutional, manufacturer, and clinician benchmarking. Monthly reports to the clinicians give valuable feedback to improve oxygenator use and patient blood gas control. Reports to the device manufacturer provide information used to evaluate the clinical consequences of small changes in the manufacturing process.

Identification of a novel human Rho protein with unusual properties: GTPase deficiency and in vivo farnesylation.

We have identified a human Rho protein, RhoE, which has unusual structural and biochemical properties that suggest a novel mechanism of regulation. Within a region that is highly conserved among small GTPases, RhoE contains amino acid differences specifically at three positions that confer oncogenicity to Ras (12, 59, and 61). As predicted by these substitutions, which impair GTP hydrolysis in Ras, RhoE binds GTP but lacks intrinsic GTPase activity and is resistant to Rho-specific GTPase-activating proteins. Replacing all three positions in RhoE with conventional amino acids completely restores GTPase activity. In vivo, RhoE is found exclusively in the GTP-bound form, suggesting that unlike previously characterized small GTPases, RhoE may be normally maintained in an activated state. Thus, amino acid changes in Ras that are selected during tumorigenesis have evolved naturally in this Rho protein and have similar consequences for catalytic function. All previously described Rho family proteins are modified by geranylgeranylation, a lipid attachment required for proper membrane localization. In contrast, the carboxy-terminal sequence of RhoE predicts that, like Ras proteins, RhoE is normally farnesylated. Indeed, we have found that RhoE in farnesylated in vivo and that this modification is required for association with the plasma membrane and with an unidentified cellular structure that may play a role in adhesion. Thus, two unusual structural features of this novel Rho protein suggest a striking evolutionary divergence from the Rho family of GTPases.

Haemodynamic and metabolic effects in diabetic ketoacidosis in rats of treatment with sodium bicarbonate or a mixture of sodium bicarbonate and sodium carbonate.

To examine factors determining the haemodynamic and metabolic responses to treatment of diabetic ketoacidosis with alkali, groups of anaesthetised and ventilated rats with either diabetic ketoacidosis (mean arterial pH 6.86-6.96, mean arterial blood pressure 63-67 mm Hg) or hypovolaemic shock due to blood withdrawal (mean pHa 7.25-7.27, mean arterial blood pressure 36-41 mm Hg) were treated with sodium chloride ('saline'), sodium bicarbonate or 'Carbicarb' (equimolar bicarbonate plus carbonate). In the diabetic ketoacidosis series, treatment with either alkali resulted in deterioration of mean arterial blood pressure and substantial elevation of blood lactate, despite a significant rise in myocardial intracellular pH determined by 31P-magnetic resonance spectroscopy. These effects were accompanied by falling trends in the ratios of myocardial phosphocreatine and ATP to inorganic phosphate. Erythrocyte 2,3-bisphosphoglycerate was virtually absent in animals with diabetic ketoacidosis of this severity and duration. In contrast, in shock due to blood withdrawal, infusion of saline or either alkali was accompanied by a transient elevation of mean arterial blood pressure and no significant change in the already elevated blood lactate; erythrocyte 2,3-bisphosphoglycerate was normal in these animals. The effect of alkalinization in rats with severe diabetic ketoacidosis was consistent with myocardial hypoxia, due to the combination of very low initial erythrocyte 2,3-bisphosphoglycerate, alkali-exacerbated left shift of the haemoglobin-oxygen dissociation curve and artificial ventilation. No evidence was found for any beneficial effect of 'Carbicarb' in either series of animals; 'Carbicarb' and sodium bicarbonate could be deleterious in metabolic acidosis of more than short duration.

Accessibility of epitopes on human transcription factor IIB in the native protein and in a complex with DNA.

Transcription factor IIB (TFIIB) plays a central role in the assembly of the RNA polymerase II initiation complex. Monoclonal antibodies (mAbs) that react with human TFIIB were prepared and used as probes to identify portions of TFIIB that are accessible when the factor is in solution and when it is contained in a complex with DNA. Seven mAbs were examined and were mapped to three regions of the TFIIB molecule. Only the mAbs that mapped to residues 52-105 inhibited transcription, immunoprecipitated recombinant TFIIB and TFIIB from HeLa cell nuclear extract (NE), and supershifted a complex containing TFIIB, the TATA-binding protein, and DNA. The mAbs that mapped to residues 1-51 and the mAb that mapped to residues 106-316 did not show activity in the functional assays, with the exception of the far N-terminal mAbs (residues 1-51), which immunoprecipitated recombinant TFIIB, but not TFIIB from HeLa cell NE. These data indicate that the region containing residues 52-105 is exposed in solution and when TFIIB is part of the preinitiation complex and that some far N-terminal epitopes are accessible on the purified protein, but become blocked when TFIIB is in HeLa cell NE or in the preinitiation complex.

The effects of sodium bicarbonate and a mixture of sodium bicarbonate and carbonate ("Carbicarb") on skeletal muscle pH and hemodynamic status in rats with hypovolemic shock.

Rats rendered hypotensive and acidotic by withdrawal of blood were treated by infusion of either an equimolar mixture of sodium bicarbonate and sodium carbonate ("Carbicarb"), sodium bicarbonate alone, or sodium chloride. Skeletal muscle intracellular pH (pHi) was measured using magnetic resonance spectroscopy from the chemical shift of the carbon-2 (C2) proton resonance of the imidazole ring of anserine. In the groups treated with alkali, arterial blood pH (pHa) was restored to normal, but no change was observed in the sodium chloride-treated animals. Despite an elevation of arterial blood partial pressure of CO2 (PaCO2) in the group treated with sodium bicarbonate, no significant change in pHi was observed in any group. Blood lactate levels, initially elevated in all groups, underwent only minor changes. In all three groups a transient and similar elevation of arterial blood pressure was observed after infusion. Differential effects of Carbicarb and sodium bicarbonate in metabolic acidosis may be dependent on the model of metabolic acidosis used, and an alteration in PaCO2 induced by alkali therapy may not be a major determinant of changes in pHi.

Effect of education on oxygen mask placement.

We have investigated the effect of nurse and patient education on oxygen mask placement after surgery. In 15 patients, each studied for 8 h, masks remained positioned correctly in two and were removed a total of 37 times in the others. Median total removal time per patient (4 min 3 s) was less than in previous studies and maximum total time of mask removal was 1 h 33 min 57 s. Masks were removed for longer than 10 min on four occasions in two patients. None of these removals was for nursing care. This is an improvement compared with previous studies.

Comparison of nasal cannulae with face mask for oxygen administration to postoperative patients.

Thirty postoperative patients were allocated randomly to receive oxygen by Hudson face mask at 4 litre min-1 (group I) or 2 litre min-1 (group II) via nasal cannulae. From 22:00 on the first night after operation, the position of the nasal cannula or face mask was observed for 8 h using video and oxyhaemoglobin saturation (SpO2) recorded simultaneously. In group I the mask remained on and positioned correctly in five patients. In the 10 other patients it was removed a total of 28 times, 17 for nursing tasks, for a median time of 2 min 39 s (range 30 s to 7 h 40 min 40 s). In group II the nasal cannula was removed once in one patient for 16 min 38 s and eight times in another for a total of 1 h 18 min 7 s. Average SpO2 with mask on was 98% (range 96.1-99.9%), with mask off 95% (range 89.8-98.8%) and with cannula 97% (range 90.8-99.3%). We conclude that nasal cannulae are more likely to remain in position than face masks and maintain an adequate saturation in most patients.

Are they getting enough? Meeting the oxygen therapy needs of postoperative patients.

Many patients require oxygen therapy as part of their postoperative care. A study to assess whether patients were actually given the supplementary oxygen prescribed showed many received only intermittent therapy. Placing more emphasis on oxygen therapy in nurse education would do much to improve its use in practice.

Video surveillance of oxygen administration by mask in postoperative patients.

Patients may not receive prescribed oxygen because the oxygen face mask becomes displaced. Using video, we have observed the position of the face mask in 20 postoperative patients and recorded the timing and the events associated with mask displacement. Correct placement of the mask was confirmed at the start of the 8-h study period from 22:00 on the first night after operation. The mask remained on continuously and positioned correctly in only one patient. In the other 19 patients, it was removed 64 times (range 1-10 times per patient). The mask was removed 45 times for nursing tasks such as mouth care and temperature measurement and these represented 70% of the total number of times that the mask was not in position. Other reasons for removal were vomiting, retching and removal by the patient. The mask remained off a median time of 6 min 55 s per episode (range 46 s to 7 h 46 min 57 s) and per patient a median of 1 h 6 min 48 s (range 1 min to 7 h 46 min 57 s). Mask removal resulted in an average decrease in oxygen saturation of 4%. Oxygen by mask at 4 litre min-1 maintained an average saturation > or = 95% in most, but not all, of the patients.