Mechanisms and etiologic factors of pulmonary edema.
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Animals↗
Biomedical subjects
F R Lewis
Publications and source records attributed to F R Lewis.
Morphologic and physiologic correlates of increased extravascular lung water.
The thermal-green dye indicator dilution method for measuring extravascular lung water (EVLW) has been extensively validated against gravimetric EVLW, but no reports to date have correlated in vivo EVLW with pulmonary physiologic parameters or postmortem lung morphologic findings. A predetermined level of hydrostatic edema was created in 12 swine by the variable inflation of a left atrial Foley balloon. EVLW, arterial and mixed venous blood gases, and mixed expired gases were before balloon inflation and periodically throughout the experiment. The animals were killed by rapid excision of the lungs, which were then reinflated and frozen in liquid nitrogen. Postmortem morphometrics were performed by photographing random sections of the lungs while still frozen. A blinded observer measured perivascular cuff width, interlobular septal width, and percent of alveoli flooded on each section. Perivascular cuff width:vessel diameter ratio correlated linearly with EVLW (r2 = 0.76; p less than 0.0001) and increased 25% for each 5 ml/kg of EVLW. Alveolar flooding did not begin until EVLW had doubled from normal to 11.4 ml/kg but then increased linearly with EVLW, reaching 60% flooding at 21 ml/kg. Increase in shunt fraction correlated linearly with increases in EVLW (r2 = 0.76; p less than 0.001) and increased approximately 10% for each EVLW increment of 5.0 ml/kg. We conclude that in vivo EVLW measurements correspond closely to more conventional morphologic and physiologic measurements and sensitively detect all levels of pulmonary edema from minimal perivascular cuffing to fulminant alveolar flooding.
Animals↗
Digital cutaneous fluorometry: correlation between blood flow and fluorescence.
Central to the use of fluorescein in vascular diagnosis is the requirement that the intensity of evoked fluorescence be proportional to blood flow. With the introduction of the digital dermofluorometer, a device that quantitates cutaneous fluorescence, establishment of this relationship has become possible. After experimentally producing measured reductions in the distal aortic flow of eight rabbits, the ratio of fluorescence in the flow-restricted and unrestricted areas was obtained by measuring hind- and forelimb fluorescence. At any time between 20 and 60 minutes following a bolus injection of sodium fluorescein (1 mg/kg body weight), there was a significant linear relationship (p less than 0.05, r greater than 0.75) between residual aortic flow and the ratio of hind-/forelimb fluorescence. Simultaneously obtained plasma fluorescein concentrations decayed rapidly by first-order kinetics with a half-life of 12.5 minutes, regardless of the degree of distal aortic occlusion. The time course of the rise and fall of cutaneous fluorescence was slower than that of the plasma fluorescein concentration, proving that interstitial rather than intravascular fluorescein was responsible for the measured fluorescence. We conclude that the intensity of tissue fluorescence is linearly related to blood flow and that conclusions regarding perfusion may be drawn from relative fluorescence at any time between 20 and 60 minutes following a bolus injection of fluorescein. Furthermore, the passage of fluorescein into the interstitium is dependent on a time-limited diffusion process, which along with flow, establishes the time to peak and the absolute amplitude of the tissue fluorescence curve.
Animals↗
Initial assessment and resuscitation.
It has been estimated that one fourth to one third of the deaths from trauma could be prevented by more effective initial care. The majority of traumatized patients who present to the emergency department do not have life-threatening injuries and may be assessed in an orderly manner. Roughly 10 per cent of patients will have life-threatening injuries, however, and speed in assessment, diagnosis, and therapy is crucial to their survival.
Airway Obstruction↗
Pupillary reactivity in circulatory arrest.
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Heart Arrest↗
Histiocytoid cardiomyopathy: a cause of sudden death in apparently healthy infants.
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Cardiomyopathies↗
Effect of inhalation injury on lung water accumulation.
Fourteen thermally injured patients with severe inhalation injury were sequentially studied with the thermal-green dye double indicator dilution technique of extravascular lung water (EVLW) measurement. Eight females and six males (average age, 49 years, and average thermal burn, 37% body surface) were studied for 2-31 days postinjury. All were burned in a closed space, had facial burns, soot in their sputum, and a mean carboxyhemoglobin level of 30%. Nine patients died, six of sepsis, one each of acute renal failure, hepatorenal syndrome, and anoxic brain damage. Mean EVLW on admission was 7.0 +/- 2.9 ml/kg and remained normal in the five survivors and in the patients dying of acute renal failure and anoxic brain damage. Six patients had increases in EVLW, caused by altered pulmonary capillary permeability in five and by elevation of hydrostatic pressures in one patient (hepatorenal death). Of the five patients with permeability edema, one appeared to result from a direct early effect of inhalation injury resulting in an EVLW of 13.3 ml/kg on admission. The other four patients had EVLW increases after the onset of sepsis, resulting in a mean EVLW of 23.2 +/0- 7.2 ml/kg at death (p less than 0.01). Seventy-one per cent of all patients developed pneumonia, which appears to have caused an EVLW increase in one patient; the other EVLW increases were caused by systemic sepsis. In our present study of 14 patients with definite severe inhalation injury only one had an early increase in EVLW directly related to the inhalation injury, an early effect on capillary permeability presumably caused by direct chemical toxicity of inhaled gases. The remaining four cases of permeability edema occurred 4-24 days postinjury and resulted from burn wound or pulmonary sepsis. We thus conclude that increases in EVLW after thermal and inhalational injury are primarily caused by systemic or pulmonary sepsis, and have a delayed onset. Early increases in EVLW may be a result of the chemical toxicity of inhaled gases but are very uncommon, moderate in degree, and are seen only with the severest cases of inhalation injury.
Adult↗
Pulmonary extravascular fluid accumulation following intracranial injury.
Previous investigations have reported an 11 to 71% incidence of pulmonary edema following CNS injury, based on post-mortem examinations. No premortem assessment to date has been made of the frequency and severity of in vivo pulmonary fluid accumulation following acute head injury. The thermal green dye technique was used to objectively determine extravascular lung water (EVLW) in 18 comatose patients with severe acute intracranial injuries resulting from trauma or spontaneous subarachnoid hemorrhage. Patients with aspiration, lung contusion, or pneumonia were excluded from the study. Control values for EVLW were obtained on admission from a group of 13 traumatized patients without head injury or evidence of pulmonary disease or injury. Intracranial injury patients who had EVLW values greater than two standard deviations above the control group mean were considered to have pulmonary edema. The incidence of pulmonary edema in this series was 50% (9/18). Extravascular lung water was determined post mortem in five patients using the gravimetric method of Pearce. The results suggest that pulmonary edema is a distinct clinical event occurring frequently after acute intracranial injury. Edema appears to be mediated by increased pulmonary microvascular permeability, and is not primarily dependent on postinjury changes in intracranial pressure or pulmonary vascular pressures.
Blood Pressure↗
Surface quantification of injected fluorescein as a predictor of flap viability.
In a laboratory model, quantitative skin-surface fluorescence has been used to reliably measure skin perfusion in ischemic random flaps and to predict viability. The method is reproducible and allows investigators to sequentially monitor soft-tissue perfusion using a fluorescent indicator. It is superior to the conventional fluorescein test (Wood's lamp method), which allows only a single subjective assessment within a 24-hour period.
Animals↗
Crystalloid versus colloid for fluid resuscitation of hypovolemic patients.
The choice of the initial asanguinous fluid--either crystalloid or colloid--used for the resuscitation of the hypovolemic patient remains controversial. Colloid supporters argue for the careful preservation of the plasma colloid osmotic pressure (PCOP) to protect the lung from pulmonary edema. A careful analysis of the Starling microvascular forces operative at the pulmonary capillary makes such an effect unlikely. In fact, the lung is relatively immune to hemodilution and any decrease in PCOP is roughly one fourth as important as increases in hydrostatic pressure in causing increased fluid exchange. A critical review of the experimental and clinical studies comparing crystalloid versus colloid resuscitation essentially shows no physiologic difference in the two solutions. Using the thermal-green dye technique of extra-vascular lung water (EVLW) measurement in twenty crystalloid resuscitated trauma (n = 10) and burn (n = 10) patients, we have specifically evaluated the pulmonary effects of profound depression of PCOP and a negative PCOP - PAWP gradient (a shorthand form of the Starling equation argued to predict the presence of pulmonary edema if + 4 mm Hg or less). Average resuscitative fluid volumes during the first two hospital days were: 31.8 litres of crystalloid and no colloid for each burn patient; and 18.5 liters of crystalloid, 21 units of blood and 1 liter of colloid (as fresh frozen plasma) for each trauma patient. EVLW remained in the normal range of 7.0 +/- 1.0 ml/kg during the first five hospital days for all patients despite profound decrease in PCOP (less than 15 mm Hg) and a low or negative PCOP - PAWP gradient. Crystalloid resuscitation clearly is not harmful to the lung and it is equally as effective as colloid resuscitation. Crystalloid is markedly less expensive than colloid and, given the greater cost of colloid without evident benefit, one wonders how their further use can be justified.
Animals↗
Panel: prehospital trauma care--stabilize or scoop and run.
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Humans↗
A single indicator technique to estimate extravascular lung water.
An estimate of extravascular thermal volume (EVTV) calculated from a single thermal indicator (SI) sampled in the pulmonary artery and the femoral artery was compared with direct gravimetric measurements of extravascular lung water (EVLW) on 47 dogs and with simultaneous double indicator (DI) dilution measurements made on 62 dogs and 38 humans with heat as the diffusible indicator and green dye as the intravascular indicator. For the gravimetric measurements the relation was EVTV(SI) = 1.00 EVLW(grav) + 61 ml r = 0.91. When compared with double indicator dilution measurements, the results were EVTV(SI) = 1.10 EVTV(DI) + 17 ml r = 0.94 for dogs and EVTV(SI) = 0.89 EVTV(DI) + 66 ml r = 0.97 for humans. A total of 1880 measurements were made over a range of EVTV(DI) from 70 to 2150 ml. The single indicator measurements of EVTV agrees with the double indicator measurements of EVTV and with the direct gravimetric measurements of EVLW and can be performed with standard catheters and without the withdrawal of blood.
Animals↗
Measurement of extravascular renal water by the thermal dye indicator dilution technique.
Simple mechanical swelling of the renal parenchyma against an unyielding renal capsule may be responsible in part for the development of oliguria and acute tubular necrosis. However, until now, renal swelling was difficult to measure, except by postmortem gravimetric techniques. A new in vivo technique, the thermal dye double indicator dilution technique, was used to assess renal swelling by measuring extravascular renal water. Ice cold indocyanine green dye solution was injected rapidly into the renal artery of 5 mongrel dogs, and the thermal dilution and dye dilution curves were recorded simultaneously by means of a thermistor catheter in the renal vein. The curves were corrected for the response time of the measuring systems, then the extravascular renal water was compared (renal blood flow multiplied by the difference in mean transit times of the thermal dilution and dye dilution curves). The results were compared to the gravimetrically determined extravascular renal water. A high correlation was found to exist between the thermal dye dilution method and the gravimetric method (r = 0.92, X = 0.65 Y + 19.8, p less than 0.05). These preliminary results are encouraging and warrant further trials, inasmuch as this technique would allow the sequential in vivo measurement of renal edema. It is therefore feasible to quantitate the effect of clinical insults, such as hypovolemic shock or sepsis, on the kidney, and to assess the value of different therapeutic interventions. A small body of evidence attempts to relate the role of simple mechanical swelling of the kidney to the pathogenesis of acute renal failure.
Animals↗
Determinants of pulmonary interstitial fluid accumulation after trauma.
We have sequentially measured the daily extravascular lung water (EVLW) changes in 16 severely traumatized patients to better define the principal etiologic factors causing post-traumatic interstitial fluid accumulation and subsequent respiratory failure. We found that severe hemorrhagic shock (mean initial BP = 40 mm Hg), massive transfusion (12.7 liters of blood), and crystalloid resuscitation with resulting hemodilution of plasma colloid osmotic pressure (PCOP) (PCOP less than or equal to 15 mmHg) do not cause EVLW accumulation. Post-traumatic elevations in EVLW were seen after lung contusion (average EVLW = 15.3 +/- 2.5 ml/kg), sepsis (average EVLW = 17.1 +/- 2.9 ml/kg) and cardiac failure (EVLW = 15.3 +/- 0.3 ml/kg). Severe hemorrhagic shock, massive transfusion, and crystalloid resuscitation with resulting hemodilution of plasma colloid oncotic pressure do not cause EVLW accumulation. Post-traumatic elevations in EVLW are seen after lung contusion, sepsis, and cardiac failure. We conclude that after trauma elevations in capillary hydrostatic pressure and capillary permeability alterations resulting from lung contusion or sepsis are the primary determinants of interstitial fluid accumulation.
Adult↗
The measurement of extravascular lung water by thermal-green dye indicator dilution.
The theory and practice of the thermal-dye indicator-dilution method for measurement of EVLW has been discussed, and all available animal data from our laboratory correlating EVTV and gravimetric EVLW have been presented. The method appears to function well over the entire range of edema seen , and to be minimally dependent on cardiac output. Thermal-indicator loss does not seem to be a significant problem and does not impair the accuracy of this method. Out results are consistent with earlier works in the field in identifying significant differences between the isotopic EVLW methods and the thermal-dye method, and it seems likely that these differences are due to the much greater diffusion rate of the thermal indicator.
Animals↗
Elevated pulmonary lymph flow and protein content during status epilepticus in sheep.
The pathophysiology of postictal pulmonary edema was investigated by inducing seizures with bicuculline in nine paralyzed, halothane-anesthetized sheep and measuring of pulmonary lymphatic flow, pulmonary arterial and left atrial pressures, and lymph and plasma albumin concentration. Pulmonary microvascular pressure and transcapillary albumin conductance were calculated. Seizures transiently (less than 15 min) elevated microvascular pressure in all animals; lymph flow increased greater than twofold in response to the increased hydrostatic driving force. However, the elevation in lymph flow, with a stable lymph-to-plasma protein ratio and doubled transcapillary albumin conductance, persisted for the duration of the experiment, more than 3 h after microvascular pressure returned to base line. These changes were neurally mediated because they were blocked by cervical spinal cord transection in four additional animals.
Animals↗