A prospective study of acute admissions in a surgical unit due to diverticular disease.

INTRODUCTION: Considerable controversy exists in the surgical literature on the most appropriate treatment modality for patients with recurrent diverticular disease. We aim to assess the clinical outcome of acute surgical admissions with diverticular disease, and in particular patients with recurrent admissions. METHODS: 100 consecutive emergency admissions with suspected diverticular disease were prospectively recruited from November 1, 2002 to May 31, 2004. RESULTS: The majority of the patients were female (64%) and the median age was 74 (45-97) years. The follow-up period was up to 30 months. Four patients with tumour and polyps as definitive diagnosis were excluded from further analysis. Fifty-four patients had a known history of diverticular disease with a median duration of 4 (range 1-40) years; 44 of them had 1-7 previous emergency admissions (median 2). Acute diverticulitis (42%) and acute rectal bleeding (23%) were the commonest presentations. Patients with complicated diverticulitis requiring an emergency operation had a median C-reactive protein of 281 mg/l compared to 58 mg/l in the conservatively treated patients with acute diverticulitis (Mann-Whitney U test, Z -3.943, p<0.001). Nine of 14 patients operated had at least two previous admissions with complications of diverticular disease. Emergency operative treatment was associated with prolonged hospital stay (21 vs. 5 days; Mann-Whitney U test, Z -4.367, p<0.001), increased morbidity and postoperative mortality. CONCLUSIONS: Symptomatic diverticular disease is associated with recurrent emergency admissions. The majority of patients who required emergency laparotomy had previous recurrent emergency admissions, which was associated with increased morbidity and prolonged hospital stay.

Important role of carotid afferents in control of breathing.

The purpose of the present study was to determine the effect on breathing in the awake state of carotid body denervation (CBD) over 1-2 wk after denervation. Studies were completed on adult goats repeatedly before and 1) for 15 days after bilateral CBD (n = 8), 2) for 7 days after unilateral CBD (n = 5), and 3) for 15 days after sham CBD (n = 3). Absence of ventilatory stimulation when NaCN was injected directly into a common carotid artery confirmed CBD. There was a significant (P < 0.01) hypoventilation during the breathing of room air after unilateral and bilateral CBD. The maximum PaCO2 increase (8 Torr for unilateral and 11 Torr for bilateral) occurred approximately 4 days after CBD. This maximum was transient because by 7 (unilateral) to 15 (bilateral) days after CBD, PaCO2 was only 3-4 Torr above control. CO2 sensitivity was attenuated from control by 60% on day 4 after bilateral CBD and by 35% on day 4 after unilateral CBD. This attenuation was transient, because CO2 sensitivity returned to control temporally similar to the return of PaCO2 during the breathing of room air. During mild and moderate treadmill exercise 1-8 days after bilateral CBD, PaCO2 was unchanged from its elevated level at rest, but, 10-15 days after CBD, PaCO2 decreased slightly from rest during exercise. These data indicate that 1) carotid afferents are an important determinant of rest and exercise breathing and ventilatory CO2 sensitivity, and 2) apparent plasticity within the ventilatory control system eventually provides compensation for chronic loss of these afferents.

Leiomyoma of the small intestine in an 11-year-old boy.

A case is reported of anaemia in an 11-year-old boy due to an ileal leiomyoma, a very rare tumour in the paediatric age group.

Effect on breathing of neuronal dysfunction in the caudal ventral medulla of goats.

It has been reported that the caudal ventrolateral medulla (VLM) is important in central chemoreception and the control of breathing. The objective of this study was to determine in adult goats the effects on breathing of neuronal dysfunction of this caudal VLM region (area L; caudal to rostral hypoglossal nerve rootlet). Thermodes were chronically implanted on the VLM to cool neurons and thereby cause neuronal dysfunction. During awake and (halothane) anesthetized states, cooling the caudal VLM for 20 s to 20 degrees C did not alter breathing (P > 0.10). However, between 20 and 30 s of cooling and during recovery from cooling 0-4 mm caudal to the rostral hypoglossal rootlet, there was a 12 (awake) to 25% (anesthetized) increase (P < 0.05) in breathing. This tachypneic hyperpnea was uniform over conditions of eucapnia, hypercapnia, and hypoxia and resulted from reduced inspiratory time that increased frequency. We conclude that in goats inhibitory neurons are located in area L and the lateral caudal ventral medulla.

Effect of carotid chemoreceptor denervation on breathing during ventrolateral medullary cooling in goats.

It has been postulated that the so-called area S of the ventrolateral medulla (VLM) integrates peripheral chemoreceptor activity; thus cooling-induced dysfunction of neurons in this VLM area should functionally eliminate carotid chemoreceptor stimulation of breathing. Accordingly, carotid chemoreceptor denervation (CBD) should not alter the breathing effects of VLM neuronal dysfunction. To test this hypothesis in awake goats, chronically implanted thermodes were used to cool the VLM and thereby cause reversible neuronal dysfunction in all or portions of VLM areas M and S. Within 5 s after initiation of cooling approximately 60-100% of areas M and S in (P < 0.05) uniformly over conditions of eupnea, hypercapnia, and hypoxia. Between 10 and 20 s of cooling, the reduction in VI was approximately 10% greater (P < 0.05) during hypercapnia than during eupnea and hypoxia. For the remaining 10 s of cooling and for approximately 1 min after cooling, VI increased to and above control for all conditions. For all conditions, CBD accentuated the depression of VI during cooling, causing VI to decrease (P < 0.05) 10-40% more than before CBD. After CBD, the greatest effect on VI of cooling was again during hypercapnia. Thus the carotid bodies in intact goats appear to sense blood gas errors caused during VLM cooling to minimize the decreases in VI. We conclude that the data from this study do not support the concept that the VLM integrates carotid chemoreceptor activity.

Differential effect of ventrolateral medullary cooling on respiratory muscles of goats.

The objective was to determine whether there is an inhomogeneous response of respiratory muscles during cooling-induced ventrolateral medullary (VLM) neuronal dysfunction in anesthetized and awake goats. Thermodes for cooling were chronically implanted on all or portions of rostral, intermediate, and caudal areas of the VLM of 16 adult goats. Electromyograms (EMGs) were obtained from chronically implanted wires in the diaphragm (di), transversus abdominis (TA), and triangularis sterni (TS) muscles. During some periods of cooling in 9 of 16 anesthetized airway-intubated goats, complete cessation of EMGdi coincided with a reduced yet sustained inspiratory flow. In six awake tracheotomized goats, VLM cooling decreased (P < 0.05) EMGdi duration and minute activity more than inspiratory duration and minute ventilation. Cooling thus decreased activation of the diaphragm more than activation of other respiratory muscles. On the other hand, during VLM cooling in 3 of 10 airway-intact awake goats, cessation of inspiratory flow coincided with sustained EMGdi, suggesting that cooling decreased stimulation of the upper airway muscles more than stimulation of the diaphragm. Finally, VLM cooling in a majority of goats decreased EMGTA and EMGTS more than EMGdi. We conclude that VLM neuronal dysfunction has a differential effect on respiratory muscles of adult anesthetized and awake goats.

Effects on breathing of ventrolateral medullary cooling in awake goats.

Our objective was to investigate the role of the ventrolateral medulla (VLM) in the control of breathing during the awake state. In 17 awake adult goats, chronically implanted thermodes were used to cool the VLM and thereby cause reversible neuronal dysfunction in all or portions of the area between the first hypoglossal rootlet and the ponto-medullary junction (so-called area M (rostral) and area S). Within 5 s after the initiation of cooling, 60-100% of areas M and S, pulmonary ventilation (VE) decreased uniformly over conditions of eucapnia, hypercapnia, hypoxia, and exercise (P < 0.05). Between 10 and 20 s of cooling, the reduction in VE was approximately 10% greater during eucapnia and hypercapnia than during hypoxia and exercise (P < 0.05). For the remaining 10 s of cooling and for about 1 min after cooling, VE increased to and above control level. Cooling only rostral area M or only caudal area M-rostral area S affected breathing qualitatively in the same manner as when 60-100% of areas M and S were cooled. However, cooling caudal area S had effects that differed significantly (P < 0.05) from more rostral cooling in that the initial decrease in VE was attenuated and the subsequent increase was accentuated. The initial uniform decreased VE during cooling suggests that superficial VLM nonchemoreceptor neurons facilitate breathing. The subsequent relatively greater effect of cooling during eucapnia and hypercapnia probably reflects dysfunction of chemoreceptor-related neurons that normally stimulate breathing. The stimulation of breathing during the later stages and after cooling may suggest that some VLM neurons inhibit breathing.

Effect of helium-induced ventilatory unloading on breathing and diaphragm EMG in awake ponies.

Two questions were addressed in this study: 1) Does respiratory resistive unloading (inspired O2 fraction = 0.21, inspired He fraction = 0.79) elicit a compensatory reduction in stimulation of the diaphragm? 2) Do diaphragm and lung afferents contribute to compensatory responses to unloading? Ten intact (I), five diaphragm-deafferented (DD), four hilar nerve-denervated (HND), and seven DD+HND adult ponies were studied at rest and during mild and moderate treadmill exercise. During steady-state unloading at rest, duration of the diaphragm electromyogram (EMGdi) was less (P < 0.05) than control in I ponies, but there were no additional significant changes in breathing or blood gases. Unloading during mild and moderate exercise increased (P < 0.05) pulmonary ventilation in all groups, and this response did not differ (P > 0.05) among the groups. With unloading during exercise, arterial PCO2 was within 1 Torr of control except in the DD+HND ponies, which were 1-2 Torr hypocapnic (P < 0.05). During exercise, the duration and rate of rise of the EMGdi were reduced (P < 0.05) below control, beginning at about the third unloaded breath. The decrease in rate of rise was usually not sustained, inasmuch as there was a gradual return toward control over 2 min of unloading. There were no consistent group differences in these EMGdi responses. We conclude that resistive unloading during mild and moderate exercise in ponies results in a transient reduction in neural drive to the diaphragm that is not critically dependent on diaphragm and pulmonary afferents.

Effect of metabolic rate on ventilatory roll-off during hypoxia.

This study was done to determine 1) whether goats demonstrate the roll-off phenomenon, i.e., a secondary decrease in minute ventilation (VE), after an initial hyperventilation during various levels of hypoxia and, if so, 2) whether roll-off could be due to changes in metabolic rate. We hypothesized that roll-off occurs in the goat during hypoxia but is not due to hypometabolism. To answer question 1, eight unanesthetized adult goats were exposed to 15-20 min of hypoxia at 0.15, 0.12, and 0.09 inspired O2 fraction (FIO2), resulting in 60, 40, and 30 Torr arterial PO2, respectively. Goats were fitted with a face mask connected to a spirometer to measure VE, and arterial blood gas samples were obtained via carotid arterial catheters. Roll-off was seen with 0.15 and 0.12 FIO2, whereas VE steadily increased with 0.09 FIO2. During hypoxia, arterial PCO2 fell 2, 3, and 7 Torr at 0.15, 0.12, and 0.09 FIO2, respectively. In the second series of experiments, nine different goats were exposed to 30 min of 0.12 FIO2. O2 consumption and CO2 production were measured five times during baseline and hypoxia. VE increased to 32% above baseline values after 2 min of hypoxia and then gradually decreased by 18%. Changes in breathing frequency and tidal volume contributed to the roll-off. O2 consumption decreased (P = 0.0029, analysis of variance) and CO2 production increased (P = 0.0027) during hypoxia, although both changes were small (< 7%) compared with the eventual 18% decrease in VE. We conclude that the adult goat demonstrates the roll-off phenomenon during moderate levels of hypoxia. (ABSTRACT TRUNCATED AT 250 WORDS)

Changes in respiratory muscle activity in ponies when end-expiratory lung volume is increased.

The objective of the present study was to determine whether lung and diaphragm afferents contribute to the changes in respiratory muscle activity when end-expiratory lung volume (EELV) is changed in ponies. We studied the responses of the diaphragm and the transversus abdominis (TA) muscles to passive increases in EELV in awake intact (I), diaphragm-deafferented (DD), pulmonary vagal- (hilar nerve) denervated (HND), and DD + HND ponies. Negative pressure of -10 or -20 cmH2O applied around the ponies' torsos [positive transrespiratory (TR) pressure] increased (P < 0.05) EELV in all ponies; the increases were more (P < 0.05) in HND and less (P < 0.05) in DD than in I ponies. In I ponies, positive TR pressure increased (P < 0.05) the rate of rise of the integrated diaphragmatic electromyogram (EMG), reflecting increased drive to the muscle. This increase was less (P < 0.05) in DD and HND than in I ponies. In DD + HND ponies, there was no significant (P > 0.10) change in drive to the diaphragm during positive TR pressure. In I ponies, positive TR pressure increased (P < 0.05) the duration and mean activity of the TA EMG. In HND and DD + HND ponies, the TA EMG was not altered by positive TR pressure. I and DD ponies decreased (P < 0.05) breathing frequency but maintained tidal volume (VT) during positive TR pressure. HND and DD+HND ponies increased breathing frequency (P < 0.05) and decreased (P < 0.05) VT during positive TR pressure. We conclude that, during positive TR pressure when the diaphragm is presumably at a mechanical disadvantage, diaphragm and vagal afferents mediate increased drive to the diaphragm to prevent VT from decreasing. In addition, during positive TR pressure, vagal afferents mediate an increase in duration of TA activity, which minimizes the increase in EELV.

Comparison of ventilatory responses to sustained reduction in arterial oxygen tension vs. content in awake ponies.

To gain insight into central and peripheral contributions to changes in breathing during hypoxia, we compared effects on breathing of reducing inspired PO2 (hypoxic hypoxia) with reducing arterial O2 content (CaO2) through elevation of carboxy-hemoglobin (COHb) (CO hypoxia). Twelve awake ponies were studied during 1 h of breathing room air followed by 6 h when COHb was increased to 25% and CaO2 was decreased by 17%. When COHb was increased, arterial PCO2 (PaCO2) increased gradually to 1.3 Torr above (P < 0.05) control level between 30 and 45 min of CO exposure. Pulmonary ventilation (VE) decreased (P = 0.09) approximately 1 liter the first 30 min of CO exposure. After approximately 45 min, PaCO2 began to decrease, steadily reaching 1.5 Torr below (P < 0.05) control level by 4.5 h of CO hypoxia. VE did not change significantly after 30 min of elevated COHb. Eight ponies were also studied during 5 h of hypoxic hypoxia (arterial PO2 approximately 40 Torr). PaCO2 decreased 5 Torr (P < 0.05) within 5 min of hypoxia and decreased another 4 Torr (P < 0.05) between 30 min and 5 h of hypoxia consistent with hypoxic ventilatory acclimatization. VE increased (P < 0.05) within 3 min of hypoxic hypoxia but then decreased (P < 0.05; VE roll off) toward control and did not increase significantly with acclimatization. Because CO and hypoxic hypoxia both decrease brain oxygenation but only hypoxic hypoxia increases carotid chemoreceptor activity, we conclude that initial hypoventilation with CO hypoxia and VE roll off with hypoxic hypoxia are consistent with hypoxic ventilatory depression within the brain. In addition, hyperventilation with prolonged CO hypoxia is consistent with a central nervous system mechanism contributing to this phase of hypoxic ventilatory acclimatization in ponies.

Effect of chronic hypoxia on breathing and EMGs of respiratory muscles in awake ponies.

Breathing, diaphragmatic and transversus abdominis electromyograms (EMGdi and EMGta, respectively), and arterial blood gases were studied during normoxia (arterial PO2 = 95 Torr) and 48 h of hypoxia (arterial PO2 = 40-50 Torr) in intact (n = 11) and carotid body-denervated (CBD, n = 9) awake ponies. In intact ponies, arterial PCO2 was 7, 5, 9, and 11 Torr below control (P less than 0.01) at 1 and 10 min and 5 and 24-48 h of hypoxia, respectively. In CBD ponies, arterial PCO2 was 3-4 Torr below control (P less than 0.01) at 4, 5, 6, and 24 h of hypoxia. In intact ponies, pulmonary ventilation, mean inspiratory flow rate, and rate of rise of EMGdi and EMGta changed in a multi-phasic fashion during hypoxia; each reached a maximum during the 1st h (P less than 0.05), declined between 1 and 5 h (P less than 0.05), and increased between 5 and 24-48 h of hypoxia. As a result of the increased drive to the diaphragm, the mean EMGdi was above control throughout hypoxia (P less than 0.05). In contrast, as a result of a sustained reduction in duration of the EMGta, the mean EMGta was below control for most of the hypoxic period. In CBD ponies, pulmonary ventilation and mean inspiratory flow rate did not change during chronic hypoxia (P greater than 0.10). In these ponies, the rate of rise of the EMGdi was less than control (P less than 0.05) for most of the hypoxic period, which resulted in the mean EMGdi to also be less than control (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory compensation for lactacidosis in ponies: role of carotid chemoreceptors and lung afferents.

We investigated changes in arterial PCO2 (PaCO2) and pulmonary ventilation (VE) in normal, carotid chemoreceptor-denervated, and hilar nerve-denervated ponies during intravenous lactic acid infusion at rest and treadmill exercise at 1.8 mph-5% grade (mild) and 1.8 mph-15% grade (moderate). Lactic acid, (0.5 M) infusion of 0.10, 0.13, and 0.20 ml.min-1.kg-1 at rest and mild and moderate exercise increased arterial [H+] linearly throughout the 10 min of acid infusion. At 10 min of infusion, arterial [H+] had increased approximately 20 nmol/l (0.2 pH units) for each condition and group. Under most conditions, the temporal pattern of PaCO2 during acid infusion was biphasic. At rest and during mild exercise in all groups, and in carotid chemoreceptor-denervated ponies during moderate exercise, PaCO2 increased approximately 2 Torr (P less than 0.05) during the first 2 min of acid infusion. However, in normal ponies during moderate exercise, PaCO2 was not changed from control in the first 2 min of infusion. Between 2 and 10 min of infusion at rest and mild and moderate exercise in all groups, there was a 5-Torr significant decrease in PaCO2, which did not differ (P greater than 0.10) between groups. VE increased between 15-30 s and 2 min of infusion, but VE changed minimally between 2 and 10 min of infusion at rest and exercise in all groups of ponies. We conclude that lactacidosis does increase VE at rest and submaximal exercise in the pony.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of cardiac denervation on cardiorespiratory responses to exercise in goats.

The purpose of this study was to determine whether intact cardiac innervation and a normal cardiovascular (CV) response are required for a normal ventilatory (VE) response to mild and moderate treadmill exercise in awake goats. Accordingly, we measured CV and respiratory responses to two levels of exercise in seven normal (N) and six cardiac-denervated (CD) goats. Evidence of surgical CD included 1) absence of a cardiac response during surgery when the left thoracic cardiac nerves, thoracic vagi, and right and left stellate ganglia were electrically stimulated, 2) total and 80% attenuation of baroreflex changes in heart rate (HR) when arterial blood pressure was raised or lowered, respectively, by infusion of vasoactive agents in awake goats, and 3) attenuation of the CV responses to exercise. At each level of exercise in the CD goats, the HR response was significantly reduced relative to the response observed before CD (P less than 0.05) and the recovery HR response was delayed. Cardiac index increased in a work rate-dependent manner in N and CD goats but was significantly lower in the CD animals (P less than 0.05). Hypotension was consistently observed during exercise following CD. There was no effect of CD on steady-state VE at any metabolic rate or on the VE-O2 uptake relationship (P greater than 0.05). The rest-to-work and work-to-work transition responses of arterial PCO2 were similar between N and CD goats, but there was a tendency toward greater hypocapnia at the exercise onset in CD goats at the highest work rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of professional competence: the clinical teacher's responsibility.

The basic function of physiotherapy education is to develop a competent clinician. A student is prepared for this role by being exposed to a variety of educational experiences, of which the most influential occur during clinical practice.

Physiotherapy - a response to challenge.

What I propose to do tonight is to look briefly at the history of physiotherapy in Australia, the factors that have determined its development, and the present challenge to the profession.

Continuing education.

As the title suggests, education of the physiotherapist should be a continuing process which starts in undergraduate days and continues throughout the whole of the person's professional life. In the past there has been little co-ordination between these two stages of education and many of the advances to be seen in undergraduate education have not flowed through to the postgraduate sphere. Yet the continuing education of the physiotherapist is of great importance to the patient and the community, to the physiotherapist herself and to the profession as a whole.

Physiotherapy in australia.

Tonight I plan to look back for a moment at the beginning of Physiotherapy in Australia, to discuss changes that have occurred primarily in education, and to think of our preparation for the future.