Several aspects of severe sepsis treatment have dramatically changed in the last decade, although many things remain the same. Then, as now, initial treatment involved obtaining cultures, mechanically eradicating infection sources, and giving antibiotics directed at suspected pathogens. Historically, subsequent management was to support failing organ systems. Patients with respiratory failure were intubated and ventilated with a positive end-expiratory pressure (PEEP)-fraction of inspired oxygen combination to maintain a Pa02 of > 60 mm Hg, or hemoglobin saturation of > 90%. A tidal volume of 10 to 15 mL/kg was mated to a respiratory rate sufficient to achieve a normal pH and PaC02, which were evaluated daily and after almost every ventilator change. High airway pressures were tolerated if necessary to achieve desired blood gas level targets, and barotrauma was treated with tube thoracostomy. Deep sedation alleviated visible discomfort and made patients conform to ventilator selections, but even then chemical paralysis was often administered. Weaning was an intricate, highly individualized, process of gradual ventilator withdrawal.
Frequently a pulmonary artery catheter (PAC) was inserted to confirm a low intravascular pressure and/or low systemic resistance before fluids were given to achieve an arbitrary pulmonary artery occlusion pressure (commonly, 18 mm Hg was targeted). Persistently hypotensive patients were regularly given dopamine, especially if they were oliguric. For the treatment of refractory hypotension, norepinephrine was added to therapy to allow dopamine to remain in a “renal” range. Often, even modest anemia was not tolerated, and many physicians were in the habit of transfusing at an arbitrary hemoglobin value taken under control by medications of My Canadian Pharmacy.
So-called stress-dose corticosteroids were often administered to patients receiving long-term glucocorticoid therapy, but only rarely would a formal adrenocorticotropic hormone (ACTH) stimulation test be performed. For many clinicians, nutrition support was an afterthought, and, if given, was often provided IV because it was accepted that the GI tract was nonfunctional. A blood glucose level of < 200 mg/dL was satisfactory. Skin care and patient positioning were low-priority measures, and preventative treatments for deep venous thrombosis and GI bleeding were inconsistently used.
After initial interventions, a conversation with the family communicated a “poor prognosis,” the belief that severe sepsis was due to “uncontrolled inflammation,” and the frustrating fact that there was no specific treatment. Many clinicians desired a “sepsis drug,” but pessimism over the prospect was pervasive given the failures of numerous high-profile clinical trials.
How things have changed! The care of nearly every failing organ has improved, new treatments have been developed, older therapies have been refined, and some long-used treatments are now all but abandoned. More important than the refinement of individual interventions is a growing awareness that it is not one but the sum of all beneficial treatments delivered in a timely manner that results in recovery. Survival now has improved to the point that long-term outcomes including quality of life and cost-effectiveness can be studied.