Group 1: Those cases in which a striking proportion of nodules demonstrate pleural or perifissural involvement characterize nodules as predominantly perilymphatic or lymphohematogenous in origin, constituting a separate arm of the algorithm (Table 1). The explanation for this pattern lies in the greater density of lymphatic channels seen in the interlobular septa and subpleural regions, including along the fissures. Once nodules are characterized as predominantly perilymphatic or lymphohematogenous in origin, further assessment requires determining whether or not nodules are distributed diffusely or are patchy or clustered, with particular attention paid to the presence or absence of the extent of axial interstitial involvement. It is recalled that the axial interstitium envelops the main pulmonary vessels and bronchi extending from the hilum outward toward the lung periphery.
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Diseases that are primarily hematogenous in origin, such as miliary infections or hematogenous metasta-ses, give rise to nodules that are randomly distributed throughout the secondary lobule, with the greatest profusion in the lung bases (Fig 3). These patterns are clearly separate from nodules that result from inhalational disorders such as occur in patients with endobronchial spread of infection or hypersensitivity pneumonitis (HP), in which nodules are predominantly centrilobular in distribution, sparing the lobular periphery (Fig 4, 5).
For the purposes of this report, multinodular disease will be defined in a patient in which there are too many nodules to easily count on routine CT scan studies, with most of these nodules measuring < 1 cm in diameter. While the most common cause of multiple pulmonary nodules is metastatic disease, it is apparent that this definition encompasses a wide range of lung diseases, both benign and malignant. It is our contention that use of a dedicated diagnostic algorithm based on characteristic high-resolution CT (HRCT) scan features coupled with clinical findings can provide either a specific diagnosis or a markedly shortened list of differential diagnoses in a majority of patients presenting with diffuse lung nodules.
Insulin decreases circulating levels of IL-1p, IL-6, migration inhibitory factor, TNF-a, and increases levels of IL- 4 and IL-10 in thermally injured rats. In lipopo-lysaccharide-treated animals, insulin suppresses TNF-a in a dose-dependant manner. Furthermore, insulin reduces proinflammatory and increases antiinflammatory cytosolic signal transduction constituents. Insulin has been shown to enhance production of endothelial nitric oxide, suppress superoxide anion generation, and inhibit myocardial apoptotic death. Hence insulin appears to have antiinflammatory effects. Because of the local effects of insulin and through its suppression of FFAs, insulin infusions cause an increase in glucose uptake in both dysfunctional and normal myocardial regions.
We have described two cases of neutropenic septic shock in which the administration of a high-dose GIK infusion was temporally associated with an improvement in hemodynamic profile, permitting cessation of inotropic support. Septic shock and the systemic inflammatory response is characterized by reversible myocardial depression, which can prove resistant to catecholamine and fluid administration. Circulating “myocardial depressant factor”—probably representing the synergistic effects of tumor necrosis factor (TNF)-a, interleukin (IL)-1p, other cytokines, and nitric oxide—is implicated in pathogenesis. Macrovascular myocardial ischemia and hypoperfusion are unlikely contributors.
An ECG showed no acute changes, and results of CT of the head were normal. A diagnosis of neutropenic septic shock secondary to hospital-acquired pneumonia was made. Broad-spectrum antimicrobials (teicoplanin, ceftazidime, amphotericin, and foscarnet) were immediately commenced, and the patient was resuscitated with sodium bicarbonate (8.4%) colloid, crystalloid, and blood products (totaling 6.5 L). Despite this, the patient remained hypotensive (80/40 mm Hg), tachycardic (110 beats/min), and anuric. Treatment was commenced with norepinephrine, and continuous venovenous hemofiltration was initiated. Over 4 h, norepinephrine doses were steadily increased to a maximum of 11 ^g/min, maintaining a MAP of > 60 mm Hg (cardiac output, 3.9 L/min; cardiac index, 2 L/min/m2; SV, 49 mL). so
Oliguria and acidemia ensued (pH 7.25; Pco2, 52 mm Hg; Po2, 74 mm Hg; base excess, -5; bicarbonate, 20 mmol/L) necessitating continuous veno-venous hemofiltration. Over the following 8 h, increasing infusions of epinephrine (rising to a maximum of 56 |xg/min) and colloid challenges (totaling 4 L) failed to significantly improve mean arterial pressure (MAP) [55 mm Hg] or cardiac output (3.1 L/min; cardiac index, 1.9 L/min/m2; SV, 26 mL; CVP, 26 mm Hg). A repeat echocardiogram showed poor left ventricular contractility with biventricular dilatation and poor ejection fraction (40%).
An infusion of GIK (30% glucose with 50 units of actrapid insulin and 80 mmol/L potassium at 1.5 mL/kg/h) was associated with a dramatic increase in cardiac output (Fig 1; Table 1). Within 4 h of commencing GIK, it was possible to start weaning the epinephrine infusion; the greatest reduction occurred in the first 14 h (from 56 to 16 ^g/min), with an infusion rate of just 6 ^g/min at 72 h, when GIK was ceased, and cessation of epinephrine at 130 h (MAP, 72 mm Hg; cardiac output, 5.5 L/min; SV, 44 mL). The patient required no further pressor support for the next 4 days. Glucose concentrations throughout the ICU stay ranged from 5 to 8 mmol/L. Ten days after hospital admission, systemic Staphylococcal infection and candidiasis developed, resulting in death.
Septic shock carries a high attendant risk of death to which impaired myocardial contractility may contribute. Recent interest in the use of glucose-insulin and potassium (GIK) infusions as therapy in ischemic myocardial depression has extended to septic myocardial depression. Few studies have demonstrated an improvement in the hemodynamics of hypodynamic septic shock on commencing GIK infusions. We describe two cases of hypo-dynamic septic shock in which such intervention was associated with an improvement in hemodynamic profile.