Dr A As we stand at the bedside, reviewing the admission laboratory findings and waiting impatiently for a chest radiograph, let us try and put these findings together. First of all, this patient presents with an acute illness with fever, chills, a cough that is productive of purulent sputum, and 3 days of watery diarrhea. At first thought this sounds like community-acquired pneumonia (CAP), possibly with an atypical pathogen. Perhaps the diarrhea is a red herring. Weight loss and left shoulder pain in a 53-year-old former smoker raises concern for lung cancer with possible postobstructive pneumonia, and we shall look for signs of volume loss or chest wall metastasis on the chest radiograph. This patient also has evidence of severe sepsis, with a left shift, and tachycardia. He has signs of impending organ failures with renal dysfunction, a creatinine level of 1.9 mg/dl, metabolic acidosis, a coagulopathy with an elevated prothrombin time and D-dimer, and low platelets that could signal early disseminated intravascular coagulation (DIC). He has respiratory failure, with an A-a gradient over 500. He is probably hemoconcentrated, and clinically we would expect him to be hypovolemic from diarrhea, high insensible losses, and poor oral intake. My immediate therapeutic concern is the tachycardia, the nature of the cardiac rhythm, and the possibility of myocardial ischemia.
Dr D I might disagree with you that this patient has severe sepsis. What if, after 2 or 3 l saline, his blood pressure, heart rate, and creatinine normalize? I think this illustrates one of the greatest triage challenges in this area, and that is differentiating infection with sepsis from another very common scenario - infection with dehydration and hypovolemia. I think the most important point is not to confuse sepsis with hypovolemia from any cause, including hemorrhage.
Dr B The firsts steps in the care of patients like this should be very systematic. Once the tachycardia was assessed and assuming the chest readiograph confirms pneumonia, I would initiate prompt antibiotic therapy based on the most likely type(s) of infection; ensure adequate hemodynamic and respiratory support; try to identify the source of infection; identify and ascertain the extent of his organ dysfunction; and, based on that, develop an overall treatment plan.
Dr C I agree - we need to treat this suspected infection. Although a chest radiograph is not initially available, there is a strong clinical suspicion for pneumonia, as a source of major infection, and empiric antibiotic coverage should be started. When the differential diagnosis includes a central nervous system infection, there is never a question in regard to early antibiotic coverage, and in fact antibiotics are started within a window of 6-8 hours. Data for most infections, especially pneumonia, have the same window of opportunity in regard to mortality. Animal models of septic shock also indicate that mortality can directly relate to time delay in antibiotics. If there is any delay in the work up, including a delay in obtaining a chest radiograph, then empiric treatment for CAP with ceftriaxone and azithromycin should be initiated.
The patient was given 2 l of normal saline and a chest radiograph was obtained. He was given a total of 18 mg adenosine with no response; and then 2.5 mg intravenous verapamil in three doses, with a decrease in heart rate to 110 beats/min. Atrial fibrillation was diagnosed. His blood pressure fell with these interventions. The chest radiograph showed a dense opacity in the right-upper lobe with patchy opacities in the right-lower lobe, the lingula, and left-upper lobe. There were no clear air bronchograms or lateral shift to suggest lobar collapse (Fig. 1).
Dr B There are now additional diagnostic data available, and clinically important interventions have been done that raise important considerations. The additional radiographic information addresses the concerns raised about the 30 lb weight loss and any chronic process that may be acutely infected. There is no clear evidence of an endobronchial lesion or airway obstruction. This, along with the history of a recent negative bone scan, makes cancer less likely. Active tuberculosis is possible, and sputum should be sent for appropriate studies. With the complaint of midsternal pleuritic chest pain, there is concern of pericardial involvement. However, there are no suggestive changes on the ECG, and the heart size looks normal, somewhat narrow, and probably under-filled, which is consistent with hypovolemia.
Dr A Do we need to consider any other diagnostic tests for CAP in a patient with severe sepsis?
Dr C It can be very helpful in cases like this to have blood and sputum cultures. It is usually possible to get a set of blood cultures in patients like this, prior to starting antibiotics. Although they do not have a high yield, they can play an important role in the treatment of the infection by identifying possible sources and unusual or resistant organisms. They can also help to identify high-risk patients.
Dr B The purist's goal is to try to establish a bacteriologic diagnosis, but the realization is that one must initially treat broadly because no single test has the sensitivity and specificity to allow one to treat narrowly. Regardless, the coverage we use includes coverage for almost every possible bacteriologic pathogen. Knowing that this patient is from the community, we do not need to consider double Gram-negative coverage, even in a septic patient. If a patient is from the community but has recently been hospitalized, is immunosuppressed, is being treated with steroids, or has structural lung disease, such as bronchiectasis, then we would consider alternative or additional antibiotic coverage to cover for Pseudomonas spp. or other resistant Gram-negative rods. For the time being there is no indication to change either the azithromycin or ceftriaxone. I agree that to try to obtain a bacteriologic diagnosis, we use blood, urine and sputum cultures, if available, and might perform bronchoscopy once the patient is hemodynamically stable.
Dr C Getting back to the ECG, the patient has a narrow complex tachycardia with a rate of 190 beats/min with 2-3 mm ST-segment depressions across the precordium. Should the heart rate be directly controlled? Could the patient be having a myocardial infarction or is he simply volume depleted? I am concerned about using adenosine before adequately addressing the patient's volume status. The initial approach should be to volume replete him aggressively and see whether the hemodynamics improve, and then address any persistent tachycardia only after he is volume replete. In this case, rate controlling agents may not be the first line of therapy, given a strong suspicion for sepsis. One question that comes up is, what if he is ischemic and you start volume resuscitating him? Is he going to go into heart failure? Does that matter? This should not be an issue. If the need arises then support him with invasive or noninvasive ventilation and get him through this. Regardless of the cause of the tachycardia, fluid load this patient.