Biomedical subjects
G J Whitman
Publications and source records attributed to G J Whitman.
Hypersensitivity vasculitis of the duodenum.
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Detection of pooled secretions above endotracheal-tube cuffs: value of plain radiographs in sheep cadavers and patients.
OBJECTIVE: Mechanical ventilation is thought to increase the risk of nosocomial pneumonia by permitting leakage of bacteria-laden gastro-oropharyngeal secretions into the upper airways. The goal of this study was (a) to validate radiographic signs of pooled secretions above endotracheal-tube cuffs (supracuff liquid) in an animal model and (b) to determine whether suctionable pooled supracuff liquid can be identified on bedside radiographs of intubated patients. MATERIALS AND METHODS: Diagnostic criteria for supracuff liquid were initially validated by three radiologists interpreting 162 randomized radiographs made in an intubated sheep cadaver. The primary criteria included (a) replacement of the normal supracuff lucency with liquid opacity and (b) the formation of a sharp interface between the lucency of the upper edge of the cuff below and the liquid above. Graded infusions of 0, 3, 8, 13, and 23 ml of saline were made in triplicate into the space above the cuff, and radiographs were evaluated for the presence or absence of saline. The validated diagnostic criteria were used by two radiologists to estimate the frequency with which pooled liquid was seen on portable chest radiographs of 47 patients undergoing elective short-term postanesthetic mechanical ventilation. RESULTS: In the sheep-cadaver model, the diagnostic criteria for supracuff liquid allowed successful differentiation between no liquid, a small amount of liquid (3-8 ml), and a large amount of liquid (13-23 ml; c2, p < .0001). In a clinical study, radiographic signs of supracuff liquid were identified in 57% of 47 patients. In a small subset of patients (n = 18), the estimated liquid volume (mean +/- SEM) was calculated to be 7.8 +/- 1.1 ml (range = 2.1-18.4 ml). CONCLUSIONS: Radiography is a sensitive means of identifying small volumes of supracuff liquid above the inflated cuffs of endotracheal tubes. Potentially contaminating liquid pooled above the cuff of an endotracheal tube can be identified in about half of patients undergoing short-term mechanical ventilation. Our results suggest the suction of the supracuff space may be a reasonable prophylactic maneuver against nosocomial pneumonia. A much larger study is suggested to investigate the actual relation between pooled supracuff liquid and the development of nosocomial pneumonia.
Endometriosis of the bladder detected by pelvic ultrasonography.
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Protection of the patent internal mammary artery by-pass graft from subsequent sternotomy.
OBJECTIVE: We describe a technique to protect the patent internal mammary artery graft from injury by repeat sternotomy. INTERVENTIONS: The internal mammary artery is dissected as far proximally as possible. The left pleural space is opened widely thus allowing the left lung to protrude through the pleural defect once mechanical ventilation is resumed. The left lung is then interposed between the internal mammary graft and the sternum. The internal mammary artery is thereby protected from adherence to the sternum and injury upon resternotomy. RESULTS: In two patients in whom this technique was employed repeat sternotomy was easily performed without injury to the internal mammary artery. CONCLUSIONS: This simple technique effectively protects the patent internal mammary artery bypass graft from injury at subsequent sternotomy.
Protecting myocardial creatine kinase activity during reperfusion improves bioenergetics and contractile function.
The exact mechanisms underlying reperfusion (RP) injury are unclear but are thought to involve toxic oxygen metabolites such as H2O2. The purpose of our study was to determine whether increasing endogenous catalase (CAT) stores would protect creatine kinase (CK) activity and improve bioenergetics and mechanical function during RP. Rats (n = 6/group) were pretreated with myristic acid (MA) or nothing 6 to 12 hr prior to cardiectomy. Hearts were Langendorff perfused and developed pressure (DP) was monitored during 25 min of 37 degrees C ischemia and 10 or 40 min of RP. CK activity was determined at baseline, end ischemia, and 40 min RP. CAT activity and H2O2 production was assayed at baseline, end ischemia, and 10 min RP. 31P NMR spectra were continuously acquired to determine ATP and phosphocreatine (PCr) concentrations. MA-pretreated hearts demonstrated elevated CAT stores (121 +/- 4%, P < 0.05). No H2O2 was produced during ischemia, and both groups generated significant but equal amounts of H2O2 at RP 10 (P < 0.001 vs preischemia (PI), P = NS between groups). By RP 40, MA-pretreated hearts recovered more DP than did control hearts (75 +/- 5% of PI vs 35 +/- 4% of PI, P < 0.001) and retained more CK activity as well (66 +/- 4% vs 52 +/- 2%, P < .05). PCr/ATP ratios of control hearts were abnormally elevated above baseline and that of MA hearts during RP (2.4 +/- 0.1 vs 1.85 +/- 0.08, P < 0.05 at RP 40).(ABSTRACT TRUNCATED AT 250 WORDS)
Mammographically detected breast cancer: location in women under 50 years old.
The mammograms of 86 women under the age of 50 years with mammographically detected cancers were reviewed. Sixty-three of these cancers (73%) were found at the periphery of the breast as defined by a zone 1 cm wide beneath the subcutaneous fat or anterior to the retromammary fat. This finding is likely due to the geometric configuration of the breast. If the breast is hemispheric, then more than 50% of the volume of breast tissue lies within this zone in a large percentage of women. Furthermore, the contrasting adjacent fat likely improves the ability to perceive an abnormality. Interaction of the terminal ducts with chemicals contained within or produced by the fat is a much less likely reason for the high percentage of cancers in this zone. Radiologists should be aware of this phenomenon and pay particular attention to this zone.
Peripheral bypass-induced pulmonary and coronary vascular injury. Association with increased levels of tumor necrosis factor.
BACKGROUND: Although cardiopulmonary bypass is associated with systemic complement activation and neutrophil sequestration, it is unclear whether bypass-induced vascular injury is localized and dependent on organ ischemia. We hypothesized that other factors perhaps related to placement of a bypass circuit or to blood perfusion of a pump-oxygenator system may produce vascular injury caused by systemically circulating mediators. In dogs, we determined whether application of a systemic venoarterial bypass circuit with pump-oxygenator perfusion but without pulmonary or cardiac flow diversion (peripheral bypass) leads to vascular injury. Since several features of the postperfusion syndrome after bypass resemble sequelae of endotoxin exposure, we also measured circulating endotoxin and tumor necrosis factor levels. METHODS AND RESULTS: Anesthetized dogs underwent 2 hours of exposure to a pump-oxygenator with peripheral venoarterial bypass. We used a double indicator measurement of pulmonary and coronary vascular permeability (protein leak index [PLI]) as indexes of vascular injury. Compared with controls (n = 7), the pulmonary PLI of dogs undergoing bypass (n = 11) increased more than threefold (18.8 +/- 2.3 vs 63.3 +/- 7.6 x 10(-4) min-1; P < .05) and the coronary PLI increased more than twofold (P < .05). The rate of disappearance of intravascular radiolabeled protein increased threefold after bypass (disappearance t1/2, 241 +/- 35 vs 84 +/- 15 minutes, control vs bypass; P < .05), suggesting a generalized increase in vascular permeability. Circulating endotoxin was detectable in blood samples from 8 of 8 bypass animals (range, 0.24 to 4.56 ng/mL) compared with 2 of 5 controls (P < .05). Tumor necrosis factor levels increased significantly with bypass (6.7 +/- 3.8 vs 146.7 +/- 33.6 U/mL, baseline vs bypass; P < .05) and were only slightly and nonsignificantly increased in controls (7.0 +/- 4.4 vs 18.2 +/- 5.9 U/mL; P = NS). Peak tumor necrosis factor but not peak endotoxin levels correlated with pulmonary and with coronary protein leak. As expected, circulating complement (CH50) levels decreased significantly during bypass, reflecting systemic complement activation. However, the levels correlated poorly with the severity of vascular injury. CONCLUSIONS: We conclude that peripheral pump-oxygenator bypass causes coronary and pulmonary vascular injury that is independent of blood flow diversion and is associated with the appearance of circulating levels of endotoxin and tumor necrosis factor, which may play a role in bypass-induced vascular injury.
The influence of respiratory acid-base status on adult pulmonary vascular resistance before and after cardiopulmonary bypass.
Respiratory acid-base status has recently been shown to affect pulmonary vascular resistance (PVR) in adults following cardiac surgery. The purpose of this study was to examine what influence cardiopulmonary bypass has on the pulmonary vascular response to changes in respiratory acid-base status. Fifteen consecutive patients undergoing aortocoronary bypass were studied under general anesthesia both before and after cardiopulmonary bypass. Arterial PCO2 was manipulated by the addition of 5 percent carbon dioxide to the breathing circuit. Both before and after bypass, PVR increased significantly as PCO2 rose from 30 mm Hg to 50 mm Hg (p < 0.05). The PVR returned to baseline as PCO2 was returned to 30 mm Hg. These data suggest that increased PVR induced by hypercarbic acidemia is not simply a result of the effects of cardiopulmonary bypass on the pulmonary circulation. Instead, we conclude that respiratory acid-base status is an important determinant of adult PVR. We believe these data may be helpful in the treatment of mechanically ventilated patients, since patients are at particular risk of having abnormalities develop in respiratory acid-base status.
Multilocular cyst of the kidney.
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Pulmonary eosinophilic granuloma.
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Influence of hydrogen ion concentration versus carbon dioxide tension on pulmonary vascular resistance after cardiac operation.
Disturbances of respiratory acid-base status are common in patients supported with mechanical ventilation of the lungs after cardiac operations. This study was conducted with two protocols. The purpose was to determine whether respiratory acid-base status influences pulmonary vascular resistance in adults after cardiac operations and whether the influence is mediated by hydrogen ion concentration or carbon dioxide tension. Patients were studied while under general anesthesia immediately after aorta-coronary bypass. In the first protocol, with seven patients, arterial carbon dioxide tension was manipulated by the addition of 5% carbon dioxide to the breathing circuit. Pulmonary vascular resistance index was determined as arterial carbon dioxide tension rose from 30 mm Hg to 50 mm Hg and back to 30 mm Hg. In the second protocol, with 10 different patients, hydrogen ion concentration was manipulated by the addition of 0.2N hydrochloric acid, sodium bicarbonate, or both as arterial carbon dioxide tension was held constant. We used analysis of variance for statistical data. The results of the first protocol showed that pulmonary vascular resistance index rose by 44% (p < 0.05) as arterial carbon dioxide tension rose from 30 to 50 mm Hg. The results of the second protocol showed that changes in pulmonary vascular resistance index were parallel to changes in hydrogen ion concentration as arterial carbon dioxide tension was held constant (p < 0.05). These data demonstrate that respiratory acid-base status is an important determinant of pulmonary vascular resistance in the adult after cardiac operations. Furthermore, these data suggest the effect is mediated by hydrogen ion concentration, not carbon dioxide tension.
Perioperative respiratory management in cardiac surgery.
The perioperative respiratory care of the cardiac surgical patient can present many challenges to the caring physician that he or she may not see among the usual patient population. Knowledge of the effects of the heart-lung machine on pulmonary performance, awareness of the anatomic changes brought on by the surgeon, and consideration of the patient's baseline cardiac and pulmonary function need to be addressed so that the pulmonary problems that they present can be managed optimally.
Breast cancer survival among women under age 50: is mammography detrimental?
Great uncertainty exists about the benefit of detecting breast cancer by mammography in women under 50 years of age. We have reviewed the survival of patients aged 49 years or less whose cancers were detected by mammography alone. 117 women under the age of 50 years were diagnosed with breast cancer between 1978 and 1991 based only on an abnormal mammogram. Ductal carcinoma in-situ (DCIS) was found in 47 (40%) of these women, whilst 70 (60%) had infiltrating ductal or infiltrating lobular carcinomas. During the same interval, 928 women in this age group presented with palpable breast cancer. DCIS was diagnosed in 82 (9%) of these women, whilst 846 (91%) had infiltrating carcinoma. Among the infiltrating cancers detected by mammography alone, 50% were stage I, whilst only 30% of the women with palpable cancers were stage I. Five-year survival for all mammographically detected cancer patients was 95%, whereas for women with palpable cancers the survival was 74% (p < 0.00005). If DCIS is not included, the corresponding survivals are 91% for mammographically detected infiltrating cancers and 72% for palpable infiltrating cancers. Only 1 woman who died among those with palpable cancer had had a mammogram before diagnosis. Our data contradict the suggestion that women under 50 are put at a survival disadvantage by undergoing mammography. We believe that investigators who have reported negative results in this age group must examine other causes for their results.
Safe intraaortic balloon pump placement through the ascending aorta using transesophageal ultrasound.
Intraaortic balloon pumping salvages a substantial number of patients who fail to be weaned from cardiopulmonary bypass after an open heart operation. Patients with severe peripheral vascular disease may require ascending aortic balloon pump insertion. We describe a simple method of direct aortic puncture for intraaortic balloon pump placement using transesophageal ultrasound as a means of avoiding complications during insertion and documenting correct balloon position.
Case 6-5--1992. Anesthetic considerations for thoracoscopic procedures.
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Primed neutrophils injure rat lung through a platelet-activating factor-dependent mechanism.
Bacterial lipopolysaccharide (LPS) promotes transient lung neutrophil sequestration. These LPS-primed neutrophils, when stimulated by an N-formyl peptide (FNLP), promote lung injury. We hypothesized that LPS-primed, FNLP-stimulated neutrophils promote lung injury through a platelet-activating factor (PAF)-dependent mechanism. Rats were pretreated with either saline or WEB2170, a PAF receptor antagonist (10 mg/kg po). One hour after pretreatment, rats were administered intraperitoneal LPS (salmonella typhimurium lipopolysaccharide, 500 micrograms/kg) followed 6 hr later by intravenous FNLP (250 micrograms/kg infused over 30 min). Two hours after the initiation of FNLP infusion, rats were sacrificed and assays were performed to measure: (1) lung neutrophil sequestration with myeloperoxidase (MPO) activity; (2) circulating neutrophil activation with nitroblue tetrazolium (NBT) staining, and (3) lung microvascular leak with 125I-albumin flux. We found that lung myeloperoxidase, circulating neutrophil NBT staining, and lung 125I-albumin flux were increased (P less than 0.05) in saline-pretreated LPS/FNLP rats, relative to control. While lung MPO remained increased (P less than 0.05) in WEB2170-pretreated LPS/FNLP rats, circulating neutrophil NBT and lung 125I-albumin flux were decreased (P less than 0.05) relative to those in saline-pretreated rats. We conclude that PAF mediates LPS/FNLP-induced neutrophil activation and lung injury, but is independent from lung neutrophil sequestration. Thus, lung neutrophil sequestration does not inevitably produce lung injury. Rather, neutrophils can accumulate in the lung without causing lung injury if neutrophil activation can be blocked.