Life threatening tension pneumoperitoneum from intestinal perforation during air reduction of intussusception.

We present a case report of a child with intussusception who underwent air reduction which was complicated by bowel perforation. Life threatening tension pneumoperitoneum developed rapidly and immediate needle decompression was life saving in this case. The pathophysiology of hyperacute abdominal compartment syndrome is discussed.

Oesophageal perforation presenting as oesophageal atresia in a premature neonate following difficult intubation.

Iatrogenic oesophageal perforation in neonates is well recognized in the medical and surgical literature with intubation injury listed as a possible contributing mechanism besides nasogastric tube placement and suctioning. Diagnosis can be difficult and sometimes confused with other entities. With early diagnosis, nonsurgical management often leads to complete resolution in neonates. We report the case of a 1-day-old premature neonate who was brought to the operating room with the preliminary diagnosis of proximal oesophageal atresia with stump perforation and distal tracheo-esophageal fistula. His intubation for respiratory distress at birth had been difficult due to Pierre-Robin sequence with micrognathia. Oesophagoscopy in the operating room revealed a patent oesophagus but perforations in the pharynx and in the proximal oesophagus with the nasogastric tube entering the pharyngeal perforation. Oesophageal perforation and the limitations of the difficult airway algorithm in small neonates are discussed.

[Perioperative endothelin, ACTH and cortisol plasma concentrations in coronary bypass patients]. / Perioperative Endothelin-, ACTH- und Kortisolplasma- konzentrationen bei Koronarbypasspatienten.

STUDY OBJECTIVE: To follow up endothelin (ET), adrenocorticotropic hormone (ACTH), and cortisol levels in patients undergoing aortocoronary bypass grafting (CABG) and to determine whether these are extracted from plasma by the pulmonary circulation. DESIGN: Convenience sample trial. SETTING: University hospital. PATIENTS: Eight male routine CABG patients without appreciable concomitant disease. INTERVENTIONS: Patients were given anaesthesia in a strictly standardised manner using etomidate, flunitrazepam, fentanyl, and pancuronium. Nitroglycerin was administered prior to cardiopulmonary bypass (CPB) at 2 mg/h and dopamine as the only catecholamine starting from CPB weaning until the end of sampling at 3.5-5 micrograms/kg.min. Samples were drawn in rapid sequence from cannulated radial and a distal pulmonary arteries (Swan-Ganz catheter) at eight sampling times starting after induction of anaesthesia and catheter placement and finishing 22 h after the end of operation. MEASUREMENTS AND RESULTS: ET levels were determined by an ET-1, 2, 3-sensitive radioimmunoassay (RIA), ACTH and cortisol by commercially available RIA kits. There was significant (P = 0.032, linear regression analysis) correlation between ET and cortisol from pulmonary arterial samples. ET was significantly (P = 0.042, two-tailed Wilcoxon test) extracted by the pulmonary circulation after induction of anaesthesia. This pulmonary-systemic arterial difference nearly disappeared intraoperatively, but tended to be restored 22 h after the end of operation at an approximately twofold increased level. CONCLUSIONS: No interrelation between ET and the hypothalamic-pituitary-adrenal axis could be established by the ET, ACTH, and cortisol plasma levels. However, the significant correlation between perioperative ET and cortisol lends further support to the hypothesis of ET release by cortisol from vascular smooth-muscle cells. There is a net pulmonary clearance of ET in patients prior to CABG that is lost intra- and early postoperatively, but tends to be restored on the 1st day thereafter at an increased level.

The effect of ephedrine bolus administration on left ventricular loading and systolic performance during high thoracic epidural anesthesia combined with general anesthesia.

We investigated the effect of ephedrine on left ventricular function in patients without cardiovascular disease under high thoracic epidural anesthesia combined with general anesthesia. Because the epidural block was extended to all cardiac segments, ephedrine was assumed to be deprived of its centrally mediated actions. Left ventricular (LV) function was assessed using transesophageal echocardiography. We measured arterial pressure (AP), heart rate (HR), LV end-systolic and end-diastolic diameter and area (ESA, EDA), wall thickness, and LV ejection time before and after intravenous ephedrine bolus administration. We calculated area ejection fraction (EFA), end-systolic wall stress (ESWS), and mean velocity of circumferential fiber shortening (mVcfc). Ephedrine had a biphasic effect on left ventricular function. It transiently decreased EDA from 18.9 to 16.5 cm2 (mean), whereas EFA and mVcfc were increased from 33% to 49%, and from 1.88 to 2.67 circumferences/s, respectively. During the second phase, ephedrine increased mean arterial pressure (MAP) from a baseline value of 62 to 87 mm Hg, EDA was restored to 19.3 cm2, and EFA and mVcfc remained above baseline (52% and 2.64 circumferences/s, respectively). ESWS was not significantly increased from baseline. We conclude that ephedrine improves left ventricular contractility, even in the presence of high thoracic epidural anesthesia, without causing relevant changes of left ventricular afterload.

Effect of phenylephrine bolus administration on left ventricular function during postural hypotension in anesthetized patients.

STUDY OBJECTIVE: To investigate the effect of intravenous (IV) phenylephrine (PHE) bolus administration on left ventricular function in patients who developed postural hypotension during isoflurane anesthesia in the head-up tilt (reverse Trendelenburg) position. DESIGN: Prospective "before-after" trial. SETTING: Operation theater of a university medical center. PATIENTS: 15 ASA physical status I and II patients without cardiovascular disorders. INTERVENTIONS: The anesthetized patients were tilted from a supine horizontal to a 30-degree reverse-Trendelenburg position. Once a steady state was achieved, PHE 3 micrograms/kg was administered as an IV bolus dose. MEASUREMENTS AND MAIN RESULTS: Transesophageal echocardiography was used to assess left ventricular function. We measured blood pressure (BP); heart rate; left ventricular end-systolic and end-diastolic area, diameter, and wall thickness; and ejection time at baseline and after tilt, immediately before and for a period of 3 minutes after PHE injection. We calculated fractional area change (FAC), mean velocity of circumferential fiber shortening (mVcf), and end-systolic wall stress. Head-up tilt caused a reduction of mean arterial pressure [from 68 to 54 mmHg (mean)], end-systolic and end-diastolic left ventricular area (from 9.7 to 6.5 cm2 and from 19.2 to 13.1 cm2, respectively) and end-systolic wall stress (from 56 to 33 10(3).dyne/cm2). FAC and mVcf remained unaltered. PHE administration restored baseline values or overcompensated the changes caused by tilt. FAC slightly decreased in response to PHE (from 0.51 to 0.43), end-systolic wall stress increased to 83 10(3).dyne/cm2, and mVcf remained unchanged. CONCLUSION: PHE bolus administration effectively restored BP and cardiac filling, which were reduced after head-up tilt, without causing a relevant impairment of left ventricular function or an increase in end-systolic wall stress above the upper normal limit.

The effect of phenylephrine bolus administration on left ventricular function during isoflurane-induced hypotension.

By using transesophageal echocardiography, we examined the effect of phenylephrine (PHE) bolus administration on left ventricular function in 16 patients with no known cardiovascular disease during isoflurane-induced hypotension. PHE was compared with norepinephrine (NE). The patients received an intravenous bolus of PHE (2 micrograms/kg) or NE (0.1 microgram/kg) in random order. The second substance was administered after levels of arterial blood pressure and heart rate returned to baseline levels. We determined fractional area change, end-systolic wall stress, and rate-corrected mean velocity of circumferential fiber shortening. Both substances effectively restored arterial blood pressure. However, after PHE, fractional area change decreased from 0.45 to 0.31 (mean) and rate corrected mean velocity of circumferential fiber shortening from 0.88 to 0.57 circumference/s, whereas both variables remained unchanged in response to NE. End-systolic wall stress increased after PHE and NE from 47.4 to 91.2 and from 54.0 to 65.2 10(3) dyne/cm2, respectively. We conclude that phenylephrine, given as intravenous bolus to patients under isoflurane hypotension, causes a transient impairment of left ventricular systolic performance.

Effect of phenylephrine bolus administration on global left ventricular function in patients with coronary artery disease and patients with valvular aortic stenosis.

BACKGROUND: Although phenylephrine bolus administration is frequently used to increase coronary perfusion pressure in patients with coronary artery disease or valvular aortic stenosis, there are no data describing its effect on left ventricular function (LVF). METHODS: Twenty patients scheduled for elective coronary artery bypass grafting (group 1) and 18 patients scheduled for elective aortic valve replacement (group 2) entered the study. The effect of phenylephrine was compared with that of norepinephrine in those patients who developed a defined degree of arterial hypotension under general anesthesia. These patients were randomized to receive an initial bolus of either phenylephrine (1 micrograms/kg) or norepinephrine (0.05 micrograms/kg) followed by a bolus of the other drug after arterial pressure and heart rate (HR) had returned to baseline. Transesophageal echocardiography was used to evaluate LVF. Arterial pressure, HR, ejection time, and LV diameter, area, and wall thickness were recorded immediately before and for 3 min after bolus administration. Fractional diameter shortening, fractional area change, mean heart rate corrected velocity of circumferential fiber shortening (mVcfc), and LV meridional end-systolic wall stress (ESWS) were calculated. RESULTS: Both substances effectively restored arterial pressure in both groups. However, in group 1, phenylephrine administration resulted in a reduction of fractional area change from 0.51 (median) to 0.39 (P = 0.0007) and a reduction of mVcfc from 1.16 to 0.61 circ/s (P = 0.0001). End-systolic wall stress increased from 98 to 186 10(3) dyne-cm-2 (P = 0.0001). Administration of norepinephrine to group 1 and administration of either substance to the group 2 patients did not cause any significant changes of LVF. CONCLUSIONS: The results indicate that phenylephrine given as an intravenous bolus to patients with CAD anesthetized with fentanyl causes a transient impairment of LV global function and that phenylephrine bolus administration is well tolerated in patients with valvular aortic stenosis.