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Restoration of spontaneous circulation after cessation of cardiopulmonary resuscitation
841
showed generalised colonisation with Pseudomonas aeruginosa and Enterobacter cloacae. 10 days later, however, after the patient had been washed in antibacterial soaps, control cultures of perineum,
axilla, nose, throat, vagina, and trachea all yielded a strain of MRSA. The organism was found to be of type 111-29 (State Institute for Public Health and Environment Protection at Bilthoven) in the Dutch typing system. In the meantime, two other patients were colonised with the same MRSA strain, necessitating the closure of the ICU. After the last colonised patient had been discharged 8 weeks later, the unit was cleaned and disinfected. Then, cultures of the environment, including sedimentation plates and air-sampling specimens, as well as nose swabs from personnel were all MRSA negative. A week after reopening of the ICU, two new patients became simultaneously colonised with the same MRSA strain. Personnel were again negative throughout this second period. Because of the two infected
patients the unit had to be closed for a further 12 weeks. The link between the first and second periods remained unclear. The ICU was cleaned, more extensively, including repeated disinfection with a phenolic detergent spray and replacement of porous tiles in the double ceiling. Cultures of dust from the tubing directly above the grilles of five of the six ICU air-exhaust channels yielded MRSA, but samples collected 1 m or deeper in the channels were negative. MRSA were also found above the grille in the air-exhaust channel in an isolation room where another MRSA patient had been nursed several months previously. The patient had been nursed for 8 weeks in this room but more than 500 repeated cultures had never yielded MRSA. However, 2 days after the air-exhaust channel culture had been taken, the exudate from his tracheostomy became purulent and culture yielded MRSA type 111-29. Conditioned air to the ICU is HEPA-filtered via an independent air-channel system after a series of coarse filters. All specimens from air inflows were negative for pathogenic bacteria. However, on the first Monday of every month, there is a practice day for the emergency electricity-generating system, leading to short interruptions in the current supply. One of these interruptions probably caused sudden negative air pressure in the exhaust channels, during which MRSA-contaminated dust was dispersed through the grille on to the patients beneath. This could even have been the result of shutting the door to the ICU with a resultant backdraught. The widespread persistence of this 111-29 strain of MRSA in
European hospitals demonstrates its excellent survival characteristics, necessitating a vigorous search and destroy strategy for elimination. Regular cleaning of grilles and air-flow channels needs to be included in maintenance schedules.
Departments of Medical Microbiology, Intensive Care, and Hospital Hygiene, De Wever Ziekenhuis, 6401 Heerlen, Netherlands
J. H. T. WAGENVOORT B. I. DAVIES E. J. A. WESTERMANN T. J. WERINK H. M. J. TOENBREKER
Restoration of spontaneous circulation after cessation of cardiopulmonary resuscitation SIR,-Despite the availability of predictive scores, decisions about proceeding with or extending cardiopulmonary resuscitation (CPR), especially for inpatients, can only be made after revival is in progress.1,2 The accuracy of decisions of teams giving advanced cardiac life-support to terminate CPR in cases of apparent death both out-of-hospital and in-hospital is unknown.3 We report unexpected sustained restoration of spontaneous circulation after cessation of advanced life-support. An 87-year-old woman with bronchial asthma and reflux oesophagitis collapsed on the ward in the presence of a nurse, who started heart massage. On arrival of the advanced life-support team, the patient was in apnoea, with dilated unreactive pupils and without carotid pulse. Laryngoscopy revealed no aspiration and the patient had fine ventricular fibrillation, which was promptly countershocked with 360 J, resulting in asystole. After administering an escalating dose of 10 mg adrenaline in total through a central line, fine ventricular fibrillation reappeared and a
second countershock restored a pulse, which was even palpable in the radial artery. Over the next 10 minutes this pulse became weaker despite another escalating dose of 10 mg adrenaline with widening QRS complexes, suggesting resistance to further advanced lifesupport. After more than 15 minutes of advanced life-support and when a central pulse was absent, it was decided to cease CPR. At extubation, she started gasping and a few minutes later, a nurse noted a radial pulse, corresponding with a systolic blood pressure of 120 mm Hg. Supraventricular complexes appeared on the electrocardiogram and after reintubation, gastric contents were aspirated via the endotracheal tube. Shortly after admission to the intensive care unit, she opened her eyes but did not respond to command. She made no further neurological recovery and died 12 days after her cardiac arrest. Two mechanisms could explain the onset of clinically detectable restoration of spontaneous circulation after stopping CPR. First, the delayed start of action of adrenaline, even though centrally administered, and second, an improved venous return after cessation of artificial ventilation. Gradual correction of acidaemia by artificial ventilation results in improved action of catecholamines and as a consequence reappearance of a supraventricular rhythm. Particularly in a rather dehydrated patient or in a patient with concealed blood loss and with raised airway pressures, spontaneous respiratory efforts may have permitted an increase of cardiac output. Similar to the perceived haemodynamics of cough CPR, negative pressure created by gasping inspiration not only causes air entry into the lungs but also augments venous return.4 To prevent aspiration in case circulation resumes after discontinuing resuscitation, we would advise against extubation of the patient immediately after interrupting artificial ventilation and to monitor the patient over the next 5 minutes. To avoid the diagnosis of refractory cardiac arrest becoming a self-fulfilling prophesy, criteria for termination of CPR need to be established with a high specificity to reduce this risk to a minimum.2 Departments of Anaesthesia and Critical Care, and of Cardiology, AZ St Jan Hospital, 8000 Brugge, Belgium
P. MARTENS Y. VANDEKERCKHOVE A. MULLIE
1. Roberts D, Landolfo K,
Light RB, Dobson K. Early predictors of mortality for hospitalized patients suffering cardiopulmonary arrest. Chest 1990; 97: 413-19 2. Martens PR, Mullie A, Buylaert W, et al. Early prediction of non-survival for patients suffering cardiac arrest: a word of caution. Intensive Care Med 1992; 18: 11-14. 3. Kellerman AL. Criteria for dead-on-arrivals, prehospital termination of CPR, and do-not-resuscitate orders. Ann Emerg Med 1993; 22: 47-51. 4. Niemann JT, Rosborough J, Hausknecht M, et al. Cough CPR: documentation of systemic perfusion in man and in an experimental model: a "window" to the mechanism of blood flow in external CPR. Crit Care Med 1980; 8: 141-46.
Spleen as autologous in-vivo blood bank in shunt surgery for portal hypertension SIR,-Portal hypertension is generally associated with congestive splenomegaly and anaemia. Treatment consists of shunt surgery with splenectomy. On average, three to four units of blood is required during the operation. Contaminated blood and blood products still enter the transfusion pool and can be a source of life-threatening infections.1 Autologous blood is used to circumvent this risk. We have used the patient’s own grossly enlarged spleen as an autologous blood bank in vivo in five cases of portal hypertension during shunt surgery. After arranging three to four units of fresh blood, these patients (aged 19-24 years) were listed for splenectomy and leinorenal shunt surgery under general anaesthesia. Written informed consent was obtained from all the patients. The right subclavean vein and left radial artery were cannulated for monitoring of central venous pressure and continuous arterial blood pressure, respectively. A continuous electrocardiogram (lead II) was set up. After surgical preparation, the spleen was explored through a left thoracoabdominal incision. The hilum of spleen was dissected and tapes were passed around the splenic artery and vein. Two doses of 3 mL adrenaline (1/50 000) were injected into the splenic artery 60 s apart. 30 s after the second dose, the splenic artery was tied and cut. Within 5 min, the splenic size was almost halved, and then the splenic vein
showed generalised colonisation with Pseudomonas aeruginosa and Enterobacter cloacae. 10 days later, however, after the patient had been washed in antibacterial soaps, control cultures of perineum,
axilla, nose, throat, vagina, and trachea all yielded a strain of MRSA. The organism was found to be of type 111-29 (State Institute for Public Health and Environment Protection at Bilthoven) in the Dutch typing system. In the meantime, two other patients were colonised with the same MRSA strain, necessitating the closure of the ICU. After the last colonised patient had been discharged 8 weeks later, the unit was cleaned and disinfected. Then, cultures of the environment, including sedimentation plates and air-sampling specimens, as well as nose swabs from personnel were all MRSA negative. A week after reopening of the ICU, two new patients became simultaneously colonised with the same MRSA strain. Personnel were again negative throughout this second period. Because of the two infected
patients the unit had to be closed for a further 12 weeks. The link between the first and second periods remained unclear. The ICU was cleaned, more extensively, including repeated disinfection with a phenolic detergent spray and replacement of porous tiles in the double ceiling. Cultures of dust from the tubing directly above the grilles of five of the six ICU air-exhaust channels yielded MRSA, but samples collected 1 m or deeper in the channels were negative. MRSA were also found above the grille in the air-exhaust channel in an isolation room where another MRSA patient had been nursed several months previously. The patient had been nursed for 8 weeks in this room but more than 500 repeated cultures had never yielded MRSA. However, 2 days after the air-exhaust channel culture had been taken, the exudate from his tracheostomy became purulent and culture yielded MRSA type 111-29. Conditioned air to the ICU is HEPA-filtered via an independent air-channel system after a series of coarse filters. All specimens from air inflows were negative for pathogenic bacteria. However, on the first Monday of every month, there is a practice day for the emergency electricity-generating system, leading to short interruptions in the current supply. One of these interruptions probably caused sudden negative air pressure in the exhaust channels, during which MRSA-contaminated dust was dispersed through the grille on to the patients beneath. This could even have been the result of shutting the door to the ICU with a resultant backdraught. The widespread persistence of this 111-29 strain of MRSA in
European hospitals demonstrates its excellent survival characteristics, necessitating a vigorous search and destroy strategy for elimination. Regular cleaning of grilles and air-flow channels needs to be included in maintenance schedules.
Departments of Medical Microbiology, Intensive Care, and Hospital Hygiene, De Wever Ziekenhuis, 6401 Heerlen, Netherlands
J. H. T. WAGENVOORT B. I. DAVIES E. J. A. WESTERMANN T. J. WERINK H. M. J. TOENBREKER
Restoration of spontaneous circulation after cessation of cardiopulmonary resuscitation SIR,-Despite the availability of predictive scores, decisions about proceeding with or extending cardiopulmonary resuscitation (CPR), especially for inpatients, can only be made after revival is in progress.1,2 The accuracy of decisions of teams giving advanced cardiac life-support to terminate CPR in cases of apparent death both out-of-hospital and in-hospital is unknown.3 We report unexpected sustained restoration of spontaneous circulation after cessation of advanced life-support. An 87-year-old woman with bronchial asthma and reflux oesophagitis collapsed on the ward in the presence of a nurse, who started heart massage. On arrival of the advanced life-support team, the patient was in apnoea, with dilated unreactive pupils and without carotid pulse. Laryngoscopy revealed no aspiration and the patient had fine ventricular fibrillation, which was promptly countershocked with 360 J, resulting in asystole. After administering an escalating dose of 10 mg adrenaline in total through a central line, fine ventricular fibrillation reappeared and a
second countershock restored a pulse, which was even palpable in the radial artery. Over the next 10 minutes this pulse became weaker despite another escalating dose of 10 mg adrenaline with widening QRS complexes, suggesting resistance to further advanced lifesupport. After more than 15 minutes of advanced life-support and when a central pulse was absent, it was decided to cease CPR. At extubation, she started gasping and a few minutes later, a nurse noted a radial pulse, corresponding with a systolic blood pressure of 120 mm Hg. Supraventricular complexes appeared on the electrocardiogram and after reintubation, gastric contents were aspirated via the endotracheal tube. Shortly after admission to the intensive care unit, she opened her eyes but did not respond to command. She made no further neurological recovery and died 12 days after her cardiac arrest. Two mechanisms could explain the onset of clinically detectable restoration of spontaneous circulation after stopping CPR. First, the delayed start of action of adrenaline, even though centrally administered, and second, an improved venous return after cessation of artificial ventilation. Gradual correction of acidaemia by artificial ventilation results in improved action of catecholamines and as a consequence reappearance of a supraventricular rhythm. Particularly in a rather dehydrated patient or in a patient with concealed blood loss and with raised airway pressures, spontaneous respiratory efforts may have permitted an increase of cardiac output. Similar to the perceived haemodynamics of cough CPR, negative pressure created by gasping inspiration not only causes air entry into the lungs but also augments venous return.4 To prevent aspiration in case circulation resumes after discontinuing resuscitation, we would advise against extubation of the patient immediately after interrupting artificial ventilation and to monitor the patient over the next 5 minutes. To avoid the diagnosis of refractory cardiac arrest becoming a self-fulfilling prophesy, criteria for termination of CPR need to be established with a high specificity to reduce this risk to a minimum.2 Departments of Anaesthesia and Critical Care, and of Cardiology, AZ St Jan Hospital, 8000 Brugge, Belgium
P. MARTENS Y. VANDEKERCKHOVE A. MULLIE
1. Roberts D, Landolfo K,
Light RB, Dobson K. Early predictors of mortality for hospitalized patients suffering cardiopulmonary arrest. Chest 1990; 97: 413-19 2. Martens PR, Mullie A, Buylaert W, et al. Early prediction of non-survival for patients suffering cardiac arrest: a word of caution. Intensive Care Med 1992; 18: 11-14. 3. Kellerman AL. Criteria for dead-on-arrivals, prehospital termination of CPR, and do-not-resuscitate orders. Ann Emerg Med 1993; 22: 47-51. 4. Niemann JT, Rosborough J, Hausknecht M, et al. Cough CPR: documentation of systemic perfusion in man and in an experimental model: a "window" to the mechanism of blood flow in external CPR. Crit Care Med 1980; 8: 141-46.
Spleen as autologous in-vivo blood bank in shunt surgery for portal hypertension SIR,-Portal hypertension is generally associated with congestive splenomegaly and anaemia. Treatment consists of shunt surgery with splenectomy. On average, three to four units of blood is required during the operation. Contaminated blood and blood products still enter the transfusion pool and can be a source of life-threatening infections.1 Autologous blood is used to circumvent this risk. We have used the patient’s own grossly enlarged spleen as an autologous blood bank in vivo in five cases of portal hypertension during shunt surgery. After arranging three to four units of fresh blood, these patients (aged 19-24 years) were listed for splenectomy and leinorenal shunt surgery under general anaesthesia. Written informed consent was obtained from all the patients. The right subclavean vein and left radial artery were cannulated for monitoring of central venous pressure and continuous arterial blood pressure, respectively. A continuous electrocardiogram (lead II) was set up. After surgical preparation, the spleen was explored through a left thoracoabdominal incision. The hilum of spleen was dissected and tapes were passed around the splenic artery and vein. Two doses of 3 mL adrenaline (1/50 000) were injected into the splenic artery 60 s apart. 30 s after the second dose, the splenic artery was tied and cut. Within 5 min, the splenic size was almost halved, and then the splenic vein