Update in Sepsis Management

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Sepsis: An update in management
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Benjamin T. Galen, MD
Christopher Sankey, MD, FHM, FACP

Sepsis is one of the oldest and most elusive syndromes in medicine, and remains a significant contributor to morbidity, mortality, and healthcare expenditure.[1] A 1992 American College of Chest Physicians and Society of Critical Care Medicine consensus conference statement introduced the systemic inflammatory response syndrome (SIRS) into the medical lexicon, along with definitions of sepsis, severe sepsis, and septic shock.[2] A 2003 consensus panel expanded the list of signs and symptoms associated with sepsis, and warned that the findings of SIRS do not differentiate sepsis from other noninfectious conditions.[3] The terminology is important, as these definitions resulted in a shift of the label of the syndrome of infection complicated by end‐organ dysfunction from sepsis to severe sepsis or septic shock. Overlap of these terms has implications for categorizing such infections for the purpose of investigation, estimating epidemiology and outcome, and coding, billing, and reimbursement.[1]

Traditional definitions of the spectrum of sepsis disorders are outlined in Table 1,[2, 3] and it is important to note that an update to these definitions is anticipated in the near future. A recent publication has called into question the sensitivity and categorical requirement of at least 2 SIRS criteria to define severe sepsis.[4] This study of more than 1 million patients from 172 intensive care units (ICUs) in Australia and New Zealand from 2000 to 2013 found that the cutoff of 2 SIRS criteria to define severe sepsis excluded 1 in 8 patients with infection and end‐organ hypoperfusion. SIRS‐negative severe sepsis patients experienced the same mortality as SIRS‐positive patients. In addition, adjusted analysis determined a stepwise increase in mortality risk associated with each additional SIRS criterion without a transition point in risk noted at 2.[4]

Traditional Definitions of Sepsis Spectrum Disorders
Definition

  • NOTE: Abbreviations: SIRS, systemic inflammatory response syndrome.

SIRS The systemic inflammatory response to a variety of severe insults. Requires 2 of the following:
Temperature >38C or 36C
Heart rate >90 beats/minute
Respiratory rate >20 breaths/minute or partial pressure of carbon dioxide (PaCO2) 32 mm Hg
White blood cell count >12,000 or 4,000 cells/L or 10% immature (band) forms
Sepsis The systemic response to infection, with SIRS criteria met in the setting of documented or strongly suspected infection
Severe sepsis Sepsis associated with organ dysfunction, hypoperfusion (including but not limited to lactic acidosis, oliguria, or acute alteration in mental status), or hypotension (systolic blood pressure 90 mm Hg or >40 mm Hg below baseline).
Septic shock Sepsis‐induced hypotension despite adequate volume resuscitation (2030 mL/kg) with perfusion abnormalities including but not limited to lactic acidosis, oliguria, or acute alteration in mental status

From 1979 through 2000, there were over 10 million reported cases of sepsis, which accounted for 1.3% of all hospitalizations in the United States.[5] Normalized to the population distribution of the 2000 US Census, there was an annualized increase in sepsis cases of 8.7%. A 2011 report revealed rates of hospitalization for patients with septicemia or sepsis in the United States more than doubled from 2000 through 2008.[6] Patients with sepsis experienced longer length of stay than other inpatients and were 8 times more likely to die during hospitalization.[6] Estimates of severe sepsis incidence are complicated by how acute organ dysfunction is defined and whether it is related to infection. As of 2001, the number of severe sepsis cases in the United States was believed to exceed 750,000 and comprise approximately 10% of ICU admissions.[1] The incidence of severe sepsis cases in the United States continues to rise.[7, 8, 9] However, a more than doubling of the use of sepsis International Classification of Diseases, Ninth Revision, Clinical Modification (ICD‐9‐CM) codes from 2004 through 2009 has also been noted.[8] Based on ICD‐9‐CM codes indicating the presence of sepsis and organ system failure, the number of severe sepsis hospitalizations per 100,000 persons in the United States increased from 143 in 2000 to 343 in 2007.[7] Total hospital costs for patients with severe sepsis were estimated to increase 57%, from $15.4 billion in 2003 to $24.3 billion in 2007.[9] The Agency for Healthcare Research and Quality considered septicemia the most expensive medical condition in the United States in a 2011 data brief, with annual aggregate hospital costs exceeding $20 billion.[10]

Although many hospitalists care for patients in the ICU and other higher acuity or step‐down units, a significant proportion of patients with severe sepsis receive care on a general medical floor.[11, 12, 13] Sepsis is also clearly not an issue restricted to patients on internal medicine services. Of over 360,000 general surgery patients from 2005 to 2007, the incidences of sepsis (2.3%) and septic shock (1.6%) greatly exceeded those of pulmonary embolism (0.3%) and myocardial infarction (0.2%). In this cohort, the need for emergency surgery and the presence of any comorbidity increased the number of sepsis cases.[14]

Despite difficulties obtaining exact estimates of case numbers, the following appears true: the spectrum of sepsis disorders (including severe sepsis and septic shock) remains a common, costly, and increasing clinical entity that is encountered by hospital medicine physicians in a variety inpatient settings. This review will provide an update for hospitalists based on many important studies that have been published since the last review of this topic in this journal.[15] The expanding evidence base in sepsis includes early goal‐directed therapy (EGDT), clinical endpoints, and bundles of care for sepsis; antibiotics (choice and timing); volume resuscitation; ICU considerations, including the use of insulin and corticosteroids; and mortality, complications, and the advent of the condition of sepsis survivorship.

EARLY GOAL‐DIRECTED THERAPY

A 2001 prospective, randomized trial of EGDT initiated in the emergency department (ED) for patients with severe sepsis and septic shock resulted in an impressive 16% reduction of in‐hospital mortality compared to standard therapy.[16] The intervention protocol included central venous catheter placement and a 500‐mL bolus of crystalloid every 30 minutes to establish a central venous pressure (CVP) of 8 to 12 mm Hg. Vasopressors were used to maintain a mean arterial pressure (MAP) greater than 65 mm Hg, and patients with a MAP greater than 90 mm Hg were given vasodilators. Patients with a central venous oxygen saturation (Scv02) of less than 70% received red blood cell transfusion with a goal hematocrit of 30%. If central venous oxygen saturation remained less than 70% despite these interventions, dobutamine was used for inotropic effect until this goal was achieved or was limited by tachycardia or hypotension.[16]

These results prompted inclusion of the specific hemodynamic targets (CVP, MAP, and Scv02) into the original 2004 Surviving Sepsis Campaign guidelines and spurred a decade of interest worldwide.[17] The incremental importance of these individual components in managing severe sepsis and septic shock has since come under scrutiny. A recent randomized trial suggested that EGDT guided by venous lactate clearance of >10% was noninferior to the goal Scv02 of >70%. However, only 10% of the study population required transfusion or dobutamine.[18, 19] Prospective ICU data on lactate‐guided therapy[20] supported the revised 2012 Surviving Sepsis Campaign (SSC) guidelines to recommend lactate normalization as part of initial resuscitation efforts, particularly when Scv02 is not available.[21] Lactate measurement may assist in recognition of cases of severe sepsis or septic shock and provide valuable triage information, as serum lactate has been shown to predict mortality from severe sepsis independent of shock or organ failure.[22] In a retrospective study of patients presenting to the ED with sepsis, a lactate >4 mmol/L was associated with progression to septic shock within 4 to 48 hours.[23]

Our understanding of the specific benefits of EGDT is far from complete, as 3 recent large prospective, multicenter, randomized trials ProCESS (Protocolized Care for Early Septic Shock), ARISE (Australasian Resuscitation In Sepsis Evaluation), and ProMISe (Protocolised Management in Sepsis) did not show EGDT protocols to be superior to usual care.[24, 25, 26] Interpreted collectively, the benefit of EGDT may not be from targeting specific physiologic parameters, but rather from the early recognition of sepsis and the appropriate use of well‐supported interventions like aggressive fluid resuscitation and early/efficacious antibiotics.[27]

Although the precise benefit of EGDT as a package versus its individual components remains in question, we have a decade of experience in delivering this care as an integral component of the bundles put forth in the SSC guidelines.[28] Observational and retrospective studies have shown increased compliance with guidelines and improved mortality after implementing these protocols, although early bundles for severe sepsis included therapies that have subsequently been called into question on an individual basis like drotrecogin alfa (activated) and glucocorticoid therapy.[29, 30, 31] The mortality benefit from sepsis bundles deserves further explanation, although education and early recognition are likely contributory.[32]

Several studies evaluated individual components of EGDT. The TRISS (Transfusion Requirements in Septic Shock) trial randomized ICU patients with septic shock to 2 different red blood cell transfusion strategies, and found no mortality benefit or reduction in ischemic events for patients transfused at a hemoglobin of 9 g/dL compared to the 7 g/dL threshold.[33] The SEPSISPAM (Assessment of Two Levels of Arterial Pressure on Survival in Patients With Septic Shock) trial compared the MAP goal of 65 to 70 mm Hg to 80 to 85 mm Hg for patients with septic shock in a randomized, multicenter trial.[34] Although there was no difference in 28‐day mortality, more atrial fibrillation was diagnosed in the higher target group. For patients with chronic hypertension, targeting the higher MAP led to less renal injury and reduced the need for renal‐replacement therapy.[34, 35] Identifying specific subsets of patients with sepsis who benefit most from particular therapies should help clinicians set patient‐specific goals and targets.

Although we can expect additional studies to provide further guidance, it is reasonable at present to adhere to protocols designed to improve timely sepsis detection and management with aggressive volume resuscitation, early/efficacious antibiotic administration, and effective infection source control.

ANTIBIOTICS AND SOURCE CONTROL

Administration of broad‐spectrum antibiotics has long been the cornerstone of sepsis management. Timely antibiotic infusion is an integral part of the 2004 and 2012 SSC guidelines,[17, 21] with the caveat that blood cultures should be obtained prior to antibiotic therapy provided that no significant delay (>45 minutes) occurs.[21] Recent studies have begun to address fundamental clinical questions, including the timing of antibiotic administration and the efficacy of empiric antibiotic choice. A landmark retrospective cohort study of ICU patients with septic shock demonstrated survival to hospital discharge was highest in patients who received antibiotics within the first hour of hypotension.[36] Survival decreased on average by 7.6% with each hour that antibiotics were delayed. Only 50% of patients with septic shock in this study received effective antibiotic therapy within 6 hours of documented hypotension.[36] A subsequent retrospective, single‐center cohort study of ED patients with severe sepsis or septic shock undergoing EGDT showed a mortality benefit when antibiotics were administered within the first hour. However, it did not demonstrate a statistically significant decline in survival on an hourly basis thereafter.[37]

A prospective, multicenter ED trial that included patients with severe sepsis in addition to septic shock[38] did not show a mortality benefit to administration of antibiotics within the first hour. In‐hospital mortality risk for patients undergoing EGDT was similar across patients in whom time to antibiotics was delayed up to 6 hours after triage.[36, 38] However, patients with severe sepsis in whom antibiotics were delayed until shock was recognized faced a statistically significant increased risk of death (odds ratio = 2.35; 95% confidence interval = 1.12‐4.53).[38, 39] A retrospective study of 28,150 patients from the SSC database demonstrated a statistically significant increase in mortality for each hour that empiric antibiotics were delayed.[40] Importantly, this trend was preserved regardless of location of sepsis diagnosis (ED, ICU, and hospital ward) and across illness severity. Though there remains debate about the critical importance of the golden hour for antibiotic administration, overall current evidence supports early empiric antibiotics in severe sepsis and septic shock.

Choosing an empiric antibiotic regimen, based on infection source and host factors, also plays a key role in sepsis outcomes. A retrospective study of patients with septic shock from 1996 to 2005 showed that inappropriate initial antibiotics (based on eventual in vitro culture sensitivities or evaluation of clinical syndrome) were used 20% of the time and resulted in a 5‐fold reduction in survival.[41] A retrospective cohort study of patients with gram‐negative bacteremia and severe sepsis or septic shock found prior antibiotic exposure within 90 days to be an independent risk factor for drug resistance and in‐hospital mortality.[42] However, careful consideration of side effects should also influence choice of initial antibiotic therapy. A Cochrane review citing 69 trials and containing 7863 subjects with sepsis compared empiric ‐lactam therapy to ‐lactamaminoglycoside combination therapy.[43] All‐cause mortality and clinical failure was similar in both groups, as was the rate of resistance. Importantly, nephrotoxicity was significantly less in the ‐lactam monotherapy group.[43]

Infection source control is an essential component of sepsis management that should occur simultaneously with antibiotic administration. The 2012 SSC guidelines promote infection source control within 12 hours of diagnosis, with consideration of the risks and benefits therein and preference for interventions with the lowest associated physiologic insult.[21] Intravascular access devices should be recognized as a common source of infection, and should be removed after alternative access has been established.[21]

FLUID RESUSCITATION

Volume resuscitation is an essential component of sepsis management, regardless of algorithm or endpoint. Three main types of nonblood product fluid resuscitation have been used: crystalloid (saline and Ringer's solutions), colloid (typically an albumin‐containing solution), and synthetic volume expanders (hydroxyethyl starch [HES] and similar compounds).

Multiple large studies confirmed the lack of a favorable riskbenefit ratio with synthetic volume expanders. Among nearly 800 patients with severe sepsis who were randomized to receive either Ringer's acetate or HES 130/0.4, a significantly higher number of patients receiving HES died (51% vs 43%, relative risk [RR] = 1.17), and required renal‐replacement therapy (22% vs 16%, RR = 1.35). One patient in each group was dialysis dependent at 90 days.[44] An additional multicenter, prospective study of HES versus 0.9% (normal) saline for fluid resuscitation in the ICU found no significant difference in mortality (18% vs 17%, P = 0.26), but did note a higher need for renal‐replacement therapy in the HES group (7.0% vs 5.8%, RR = 1.21).[45] A systematic review incorporating 9 trials that randomized approximately 3400 patients with sepsis receiving either HES, crystalloid, or colloid showed no difference in mortality, although there was an excess risk for renal‐replacement therapy (RR = 1.36), serious adverse events (RR = 1.30), and red blood cell transfusion (RR = 1.29) in patients receiving HES.[46] A second, larger systematic review concluded that HES was associated with an increased mortality compared with crystalloids, albumin, or gelatin (RR = 1.09). Additionally, an increase in renal failure (RR = 1.27) and renal‐replacement therapy (RR = 1.32) was also noted.[47]

The debate between crystalloid and colloid (namely albumin) for fluid resuscitation is ongoing, with recent important additions to the literature. The SAFE (Saline Versus Albumin Fluid Evaluation) study investigators in 2004 randomized nearly 7000 patients to receive either 4% albumin solution or normal saline. At 28 days, no significant differences were found in mortality, new organ failure, ICU and hospital length of stay, days of mechanical ventilation, or days of renal‐replacement therapy.[48] In 2014, another multicenter prospective study of 1800 patients with severe sepsis or septic shock in 100 ICUs in Italy compared 20% albumin and crystalloid solution to crystalloid solution alone. Mortality, end‐organ dysfunction, and ICU length of stay did not differ between groups.[49] Two 2014 systematic reviews and meta‐analyses on fluid resuscitation produced somewhat differing conclusions. Patel et al. evaluated data from 16 randomized trials including more than 4000 patients receiving albumin for volume resuscitation in adults with sepsis. Albumin provided no significant survival advantage in total or in any subgroup, regardless of severity of illness or baseline albumin level, thus arguing against its routine use.[50] Rochwerg et al. evaluated 14 studies with approximately 19,000 patients using Bayesian network meta‐analysis technique. This study concluded that albumin is associated with reduced mortality compared with other fluids, and also that balanced crystalloids (eg, Ringer's lactate and similar) may have lower mortality than normal saline.[51] A chloride‐restrictive resuscitation approach has also been associated with a lower incidence of acute kidney injury in critically ill adults.[52]

The SSC confirmed its recommendations of a minimum of 30 mL/kg of crystalloids as the initial fluid of choice in sepsis in 2012, but added a suggestion for the addition of albumin in patients requiring substantial amounts of crystalloid.[21] The currently available data suggest crystalloid fluids to be the best‐supported initial fluid in the management of sepsis, and that synthetic colloids should be avoided. Prospective data are still required to answer questions regarding the potential advantages of albumin or balanced and/or chloride‐restricted crystalloids.

ICU CONSIDERATIONS

Appropriate management of patients with the syndrome of sepsis, severe sepsis, and septic shock on the hospital ward requires a working knowledge of recent research conducted in the ICU setting. Although conclusions based on data from patients with septic shock might not be generalizable to less severe cases of sepsis, recent trials on glucose control and corticosteroids deserve consideration.

Intensive insulin treatment in the medical ICU is no longer standard practice. In the NICE‐SUGAR (Normoglycaemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation) trial, a large, multicenter randomized controlled trial of ICU patients, close to 20% of patients had severe sepsis at the time of randomization.[53] This subgroup did not benefit from intensive glucose control (a target of 81108 mg/dL) in terms of 90‐day mortality.[53] In contrast to prior studies of glycemic control in the critically ill, the intensive treatment group overall suffered increased mortality.[54] The COIITSS (Combination of Corticotherapy and Intensive Insulin Therapy for Septic Shock) trial looked at intensive insulin therapy in patients with septic shock being treated with corticosteroids, a group particularly at risk for hyperglycemia. In this study, intensive insulin therapy did not improve in‐hospital mortality.[55] Based on these and other ICU data, the current SSC recommendation is to target a blood glucose of 180 mg/dL for patients with severe sepsis.[21, 56]

The use of corticosteroids to treat the host response in septic shock has been re‐evaluated.[57] The 2004 SSC guidelines recommended hydrocortisone therapy for 7 days in patients with septic shock requiring vasopressor support after fluid resuscitation.[17] This recommendation was based on data from a placebo‐controlled multicenter trial in France that showed improved shock reversal and reduced mortality in patients with septic shock who were treated with hydrocortisone and fludricortisone.[58] Of note, these patients were enrolled on the basis of hypotension despite intravenous fluids and the initiation of 1 vasopressor. The benefit of corticosteroids was seen only in patients deemed to have relative adrenal insufficiency based on response corticotropin testing.[58] However, the CORTICUS (Corticosteroid Therapy of Septic Shock) study, a subsequent multicenter, placebo‐controlled, randomized controlled trial failed to show a benefit to corticotropin testing in identifying patients with septic shock who would benefit from corticorsteroids.[59] The corticosteroid treatment arm similarly benefited from faster shock reversal, but at the expense of increased superinfection.[59] Although underpowered, CORTICUS did not show a survival benefit to corticosteroids in septic shock.[59] The most recent SSC guidelines do not recommend corticotropin (adrenocorticotropic hormone) stimulation testing and do not advise corticosteroids in septic shock if fluid resuscitation and vasopressor therapy restore hemodynamic stability during initial resuscitation.[21] Future studies may clarify subpopulations of patients with sepsis who benefit from corticosteroids.

OUTCOMES: MORTALITY AND COMPLICATIONS

An understanding of the currently available information regarding the morbidity and mortality associated with severe sepsis is essential for the practicing hospitalist. Whether transferring care of patients to or receiving patients from the ICU, hospitalists must lead discussions with patients and families regarding prognosis, especially as it informs disposition. Hospitalists are often asked to make projections on outcome as well as the timing and venue of disposition. Clarification of patient wishes and goals of care remains an essential first step in the care of septic patients. Recently published studies provide prognostic information, including mortality (both short and long term) as well as complications associated with severe sepsis.

The attributable mortality for severe sepsis has been predominantly reported to date as short‐term (usually in‐hospital). A meta‐analysis of US patients from 1991 to 2009 demonstrated a 3% annual decline in the short‐term (28 day) mortality from severe sepsis using 2 previously validated algorithms. Data from 36 trials (and approximately 14,000 patients) revealed a decrease in mortality from 47% in the period from 1991 to 1995 to 29% from 2006 to 2009.[60] Although the methods employed (sepsis definitions and ICD‐9‐CM codes) can have a significant impact on estimates of mortality, these results corroborate a progressive decline in short‐term mortality from severe sepsis in the United States between 2004 and 2009 using 4 validated algorithms.[8] Outside the United States, a recent retrospective analysis of more than 1 million patients with severe sepsis treated in the ICU in Australia and New Zealand from 2000 to 2012 also demonstrated a decrease in adjusted in‐hospital mortality. In this study, short‐term mortality declined yearly, with an odds ratio of death of 0.49 in 2012 compared with 2000.[61] Hospital case volume has also been shown to impact rates of inpatient death, with higher‐volume centers demonstrating lower mortality attributed to severe sepsis.[62, 63]

The sufficiency of short‐term mortality as the sole metric for severe sepsis outcome has been more recently questioned.[64, 65] The extent to which full recovery and significant morbidity are affected relative to the change in death rate is unknown, and as such, more data on morbidity and longer‐term mortality are necessary. A Danish study examined data from several registries of patients with severe sepsis. Compared with community‐matched controls, patients with severe sepsis had an increased risk of death at 30 days (hazard ratio [HR] = 90.8), from 30 days to 1 year (HR = 2.7), and 1 to 4 years (HR = 2.3) after discharge.[66] Older survivors of severe sepsis also appear to have higher healthcare utilization in the year following discharge. An analysis of older severe sepsis survivors showed a striking increase in healthcare use relative to their prior resource use, driven primarily by higher number of days in inpatient healthcare facilities. Survivors of severe sepsis also had a significantly higher 90‐day and 1‐year mortality than matched controls.[67]

Increased attention is currently being given to sepsis‐related complications, especially functional and cognitive impairments in older patients. Sepsis survivorship is a swiftly mounting public health issue for older Americans.[68] An 8‐year follow‐up of older sepsis survivors demonstrated a significant increase in the odds of both physical and cognitive dysfunction. During this period, moderate‐to‐severe cognitive dysfunction increased 3‐fold (6.1% before sepsis, 16.7% after).[69] The mechanism by which this dysfunction occurs is unknown, as are the relative contributions of infection site/etiology, ICU length of stay, and extent of organ dysfunction. New functional impairment has been demonstrated in patients with severe sepsis initially admitted to a general floor, even with good baseline function,[12] as well as decreased quality of life in sepsis survivors.[65, 70] Another study showed more admissions complicated by severe sepsis resulted in discharge to a long‐term care facility in 2007 compared to 2000.[7]

Additional organ‐specific consequences of severe sepsis have also been recently suggested. A retrospective analysis showed an increase in the incidence of new‐onset atrial fibrillation in severe sepsis, with an associated increase in risk of in‐hospital stroke and death. New‐onset atrial fibrillation was present in 5.9% of patients with severe sepsis, compared with 0.65% in patients without. Severe sepsis patients with new‐onset atrial fibrillation had an increased risk of in‐hospital stroke (adjusted odds ratio = 2.70) and mortality (adjusted RR = 1.07).[71] These findings suggest association only, and further investigation is warranted. It remains to be seen whether interventions to restore sinus rhythm or anticoagulation are warranted. Preoperative sepsis (within 48 hours) has also been proposed as a risk for postoperative (30 day) arterial (myocardial infarction, stroke) and venous (deep venous thrombosis, pulmonary embolism) thromboembolism. The authors of this study suggest deferral of elective surgery or specific attention to postoperative thromboprophylaxis in patients in whom procedures must occur.[72] This has particular relevance for those septic patients in whom surgical source control is indicated.

Estimates regarding mortality and specific complications attributable to severe sepsis are ongoing, though clearly with a new focus upon metrics other than short‐term mortality. Furthermore, recent data to suggest source of infection as a major driver of mortality in septic shock[73] may contribute to the evolution of the conceptualization of sepsis similar to that of cancer: a heterogeneous collection of disease, among which mortality is determined by specific subtypes. At present, this much appears clear: the previously held notion that survival of a septic insult is unlikely to have future implications is under siege.[74] The extent to which complications and increased longer‐term mortality may reflect generally poorer health at the time of infection versus a sequelae of the survived episode itself is not yet known.

CONCLUSIONS

The past decade of sepsis research has led to significant findings that will change clinical practice for hospital medicine practitioners. Although the incidence of severe sepsis in the United States has continued to rise, in‐hospital mortality has declined; in this context, the management of the spectrum of sepsis disorders is no longer restricted to the ICU, and the entity of sepsis survivorship has blossomed. Prompt recognition of sepsis and improvements in supportive care are likely responsible for improved patient outcomes. EGDT has been called into question as a protocol whose benefit lies not in specific targets or endpoints, but rather in the early recognition of sepsis, appropriate fluid resuscitation, and early/effective antibiotics. Synthetic volume expanders, intensive insulin therapy, and routine use of corticosteroids are no longer recommended.

Hospitalists are a critical link in providing timely, evidence‐based care for patients with sepsis from initial recognition to post‐ICU recovery. Specialized care for the survivors of septic shock is a burgeoning area, and hospitalists are integral in the management of the sequelae of multiorgan failure.

Disclosure: Nothing to report.

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  42. Johnson MT, Reichley R, Hoppe‐Bauer J, Dunne WM, Micek S, Kollef M. Impact of previous antibiotic therapy on outcome of gram‐negative severe sepsis. Crit Care Med. 2011;39(8):1859–1865.
  43. Paul M, Lador A, Grozinsky‐Glasberg S, Leibovici L. Beta lactam antibiotic monotherapy versus beta lactam‐aminoglycoside antibiotic combination therapy for sepsis. Cochrane Database Syst Rev. 2014;1:CD003344.
  44. Perner A, Haase N, Guttormsen AB, et al. Hydroxyethyl starch 130/0.42 versus ringer's acetate in severe sepsis. N Engl J Med. 2012;367(2):124–134.
  45. Myburgh JA, Finfer S, Bellomo R, et al.; CHEST Investigators; Australian and New Zealand Intensive Care Society Clinical Trials Group. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med. 2012;367(20):1901–1911.
  46. Haase N, Perner A, Hennings LI, et al. Hydroxyethyl starch 130/0.38–0.45 versus crystalloid or albumin in patients with sepsis: systematic review with meta‐analysis and trial sequential analysis. BMJ. 2013;346:f839.
  47. Zarychanski R, Abou‐Setta AM, Turgeon AF, et al. Association of hydroxyethyl starch administration with mortality and acute kidney injury in critically ill patients requiring volume resuscitation: a systematic review and meta‐analysis. JAMA. 2013;309(7):678–688.
  48. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R; SAFE Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350(22):2247–2256.
  49. Caironi P, Tognoni G, Masson S, et al. Albumin replacement in patients with severe sepsis or septic shock. N Engl J Med. 2014;370(15):1412–1421.
  50. Patel A, Laffan MA, Waheed U, Brett SJ. Randomised trials of human albumin for adults with sepsis: systematic review and meta‐analysis with trial sequential analysis of all‐cause mortality. BMJ. 2014;349:g4561.
  51. Rochwerg B, Alhazzani W, Sindi A, et al. Fluid resuscitation in sepsis: a systematic review and network meta‐analysis. Ann Intern Med. 2014;161(5):347–355.
  52. Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M. Association between a chloride‐liberal vs chloride‐restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA. 2012;308(15):1566–1572.
  53. NICE‐SUGAR Study Investigators, Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283–1297.
  54. Inzucchi SE, Siegel MD. Glucose control in the ICU—how tight is too tight? N Engl J Med. 2009;360(13):1346–1349.
  55. COIITSS Study Investigators, Annane D, Cariou A, Maxime V, et al. Corticosteroid treatment and intensive insulin therapy for septic shock in adults: a randomized controlled trial. JAMA. 2010;303(4):341–348.
  56. Griesdale DE, Souza RJ, Dam RM, et al. Intensive insulin therapy and mortality among critically ill patients: a meta‐analysis including NICE‐SUGAR study data. CMAJ. 2009;180(8):821–827.
  57. Annane D, Bellissant E, Bollaert PE, et al. Corticosteroids in the treatment of severe sepsis and septic shock in adults: a systematic review. JAMA. 2009;301(22):2362–2375.
  58. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002;288(7):862–871.
  59. Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008;358(2):111–124.
  60. Stevenson EK, Rubenstein AR, Radin GT, Wiener RS, Walkey AJ. Two decades of mortality trends among patients with severe sepsis: a comparative meta‐analysis. Crit Care Med. 2014;42(3):625–631.
  61. Kaukonen KM, Bailey M, Suzuki S, Pilcher D, Bellomo R. Mortality related to severe sepsis and septic shock among critically ill patients in Australia and New Zealand, 2000–2012. JAMA. 2014;311(13):1308–1316.
  62. Gaieski DF, Edwards M, Kallan MJ, Mikkelsen ME, Goyal M, Carr BG. The relationship between hospital volume and mortality in severe sepsis. Am J Respir Crit Care Med. 2014;190(6):665–674.
  63. Walkey AJ, Wiener RS. Hospital case volume and outcomes among patients hospitalized with severe sepsis. Am J Respir Crit Care Med. 2014;189(5):548–555.
  64. Iwashyna TJ, Angus DC. Declining case fatality rates for severe sepsis: Good data bring good news with ambiguous implications. JAMA. 2014;311(13):1295–1297.
  65. Winters BD, Eberlein M, Leung J, Needham DM, Pronovost PJ, Sevransky JE. Long‐term mortality and quality of life in sepsis: a systematic review. Crit Care Med. 2010;38(5):1276–1283.
  66. Storgaard M, Hallas J, Gahrn‐Hansen B, Pedersen SS, Pedersen C, Lassen AT. Short‐ and long‐term mortality in patients with community‐acquired severe sepsis and septic shock. Scand J Infect Dis. 2013;45(8):577–583.
  67. Prescott HC, Langa KM, Liu V, Escobar GJ, Iwashyna TJ. Increased 1‐year healthcare use in survivors of severe sepsis. Am J Respir Crit Care Med. 2014;190(1):62–69.
  68. Iwashyna TJ, Cooke CR, Wunsch H, Kahn JM. Population burden of long‐term survivorship after severe sepsis in older Americans. J Am Geriatr Soc. 2012;60(6):1070–1077.
  69. Iwashyna TJ, Ely EW, Smith DM, Langa KM. Long‐term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787–1794.
  70. Karlsson S, Ruokonen E, Varpula T, Ala‐Kokko TI, Pettilä V; Finnsepsis Study Group. Long‐term outcome and quality‐adjusted life years after severe sepsis. Crit Care Med. 2009;37(4):1268–1274.
  71. Walkey AJ, Wiener RS, Ghobrial JM, Curtis LH, Benjamin EJ. Incident stroke and mortality associated with new‐onset atrial fibrillation in patients hospitalized with severe sepsis. JAMA. 2011;306(20):2248–2254.
  72. Donze JD, Ridker PM, Finlayson SR, Bates DW. Impact of sepsis on risk of postoperative arterial and venous thromboses: large prospective cohort study. BMJ. 2014;349:g5334.
  73. Leligdowicz A, Dodek PM, Norena M, Wong H, Kumar A, Kumar A; Co‐operative Antimicrobial Therapy of Septic Shock Database Research Group. Association between source of infection and hospital mortality in patients who have septic shock. Am J Respir Crit Care Med. 2014;189(10):1204–1213.
  74. Angus DC. The lingering consequences of sepsis: a hidden public health disaster? JAMA. 2010;304(16):1833–1834.
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Journal of Hospital Medicine - 10(11)
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Author(s)
Benjamin T. Galen, MD
Christopher Sankey, MD, FHM, FACP
Author(s)
Benjamin T. Galen, MD
Christopher Sankey, MD, FHM, FACP
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Supporting Information (1)
Article PDF
jhm2435.pdf
Article PDF
jhm2435.pdf

Sepsis is one of the oldest and most elusive syndromes in medicine, and remains a significant contributor to morbidity, mortality, and healthcare expenditure.[1] A 1992 American College of Chest Physicians and Society of Critical Care Medicine consensus conference statement introduced the systemic inflammatory response syndrome (SIRS) into the medical lexicon, along with definitions of sepsis, severe sepsis, and septic shock.[2] A 2003 consensus panel expanded the list of signs and symptoms associated with sepsis, and warned that the findings of SIRS do not differentiate sepsis from other noninfectious conditions.[3] The terminology is important, as these definitions resulted in a shift of the label of the syndrome of infection complicated by end‐organ dysfunction from sepsis to severe sepsis or septic shock. Overlap of these terms has implications for categorizing such infections for the purpose of investigation, estimating epidemiology and outcome, and coding, billing, and reimbursement.[1]

Traditional definitions of the spectrum of sepsis disorders are outlined in Table 1,[2, 3] and it is important to note that an update to these definitions is anticipated in the near future. A recent publication has called into question the sensitivity and categorical requirement of at least 2 SIRS criteria to define severe sepsis.[4] This study of more than 1 million patients from 172 intensive care units (ICUs) in Australia and New Zealand from 2000 to 2013 found that the cutoff of 2 SIRS criteria to define severe sepsis excluded 1 in 8 patients with infection and end‐organ hypoperfusion. SIRS‐negative severe sepsis patients experienced the same mortality as SIRS‐positive patients. In addition, adjusted analysis determined a stepwise increase in mortality risk associated with each additional SIRS criterion without a transition point in risk noted at 2.[4]

Traditional Definitions of Sepsis Spectrum Disorders
Definition

  • NOTE: Abbreviations: SIRS, systemic inflammatory response syndrome.

SIRS The systemic inflammatory response to a variety of severe insults. Requires 2 of the following:
Temperature >38C or 36C
Heart rate >90 beats/minute
Respiratory rate >20 breaths/minute or partial pressure of carbon dioxide (PaCO2) 32 mm Hg
White blood cell count >12,000 or 4,000 cells/L or 10% immature (band) forms
Sepsis The systemic response to infection, with SIRS criteria met in the setting of documented or strongly suspected infection
Severe sepsis Sepsis associated with organ dysfunction, hypoperfusion (including but not limited to lactic acidosis, oliguria, or acute alteration in mental status), or hypotension (systolic blood pressure 90 mm Hg or >40 mm Hg below baseline).
Septic shock Sepsis‐induced hypotension despite adequate volume resuscitation (2030 mL/kg) with perfusion abnormalities including but not limited to lactic acidosis, oliguria, or acute alteration in mental status

From 1979 through 2000, there were over 10 million reported cases of sepsis, which accounted for 1.3% of all hospitalizations in the United States.[5] Normalized to the population distribution of the 2000 US Census, there was an annualized increase in sepsis cases of 8.7%. A 2011 report revealed rates of hospitalization for patients with septicemia or sepsis in the United States more than doubled from 2000 through 2008.[6] Patients with sepsis experienced longer length of stay than other inpatients and were 8 times more likely to die during hospitalization.[6] Estimates of severe sepsis incidence are complicated by how acute organ dysfunction is defined and whether it is related to infection. As of 2001, the number of severe sepsis cases in the United States was believed to exceed 750,000 and comprise approximately 10% of ICU admissions.[1] The incidence of severe sepsis cases in the United States continues to rise.[7, 8, 9] However, a more than doubling of the use of sepsis International Classification of Diseases, Ninth Revision, Clinical Modification (ICD‐9‐CM) codes from 2004 through 2009 has also been noted.[8] Based on ICD‐9‐CM codes indicating the presence of sepsis and organ system failure, the number of severe sepsis hospitalizations per 100,000 persons in the United States increased from 143 in 2000 to 343 in 2007.[7] Total hospital costs for patients with severe sepsis were estimated to increase 57%, from $15.4 billion in 2003 to $24.3 billion in 2007.[9] The Agency for Healthcare Research and Quality considered septicemia the most expensive medical condition in the United States in a 2011 data brief, with annual aggregate hospital costs exceeding $20 billion.[10]

Although many hospitalists care for patients in the ICU and other higher acuity or step‐down units, a significant proportion of patients with severe sepsis receive care on a general medical floor.[11, 12, 13] Sepsis is also clearly not an issue restricted to patients on internal medicine services. Of over 360,000 general surgery patients from 2005 to 2007, the incidences of sepsis (2.3%) and septic shock (1.6%) greatly exceeded those of pulmonary embolism (0.3%) and myocardial infarction (0.2%). In this cohort, the need for emergency surgery and the presence of any comorbidity increased the number of sepsis cases.[14]

Despite difficulties obtaining exact estimates of case numbers, the following appears true: the spectrum of sepsis disorders (including severe sepsis and septic shock) remains a common, costly, and increasing clinical entity that is encountered by hospital medicine physicians in a variety inpatient settings. This review will provide an update for hospitalists based on many important studies that have been published since the last review of this topic in this journal.[15] The expanding evidence base in sepsis includes early goal‐directed therapy (EGDT), clinical endpoints, and bundles of care for sepsis; antibiotics (choice and timing); volume resuscitation; ICU considerations, including the use of insulin and corticosteroids; and mortality, complications, and the advent of the condition of sepsis survivorship.

EARLY GOAL‐DIRECTED THERAPY

A 2001 prospective, randomized trial of EGDT initiated in the emergency department (ED) for patients with severe sepsis and septic shock resulted in an impressive 16% reduction of in‐hospital mortality compared to standard therapy.[16] The intervention protocol included central venous catheter placement and a 500‐mL bolus of crystalloid every 30 minutes to establish a central venous pressure (CVP) of 8 to 12 mm Hg. Vasopressors were used to maintain a mean arterial pressure (MAP) greater than 65 mm Hg, and patients with a MAP greater than 90 mm Hg were given vasodilators. Patients with a central venous oxygen saturation (Scv02) of less than 70% received red blood cell transfusion with a goal hematocrit of 30%. If central venous oxygen saturation remained less than 70% despite these interventions, dobutamine was used for inotropic effect until this goal was achieved or was limited by tachycardia or hypotension.[16]

These results prompted inclusion of the specific hemodynamic targets (CVP, MAP, and Scv02) into the original 2004 Surviving Sepsis Campaign guidelines and spurred a decade of interest worldwide.[17] The incremental importance of these individual components in managing severe sepsis and septic shock has since come under scrutiny. A recent randomized trial suggested that EGDT guided by venous lactate clearance of >10% was noninferior to the goal Scv02 of >70%. However, only 10% of the study population required transfusion or dobutamine.[18, 19] Prospective ICU data on lactate‐guided therapy[20] supported the revised 2012 Surviving Sepsis Campaign (SSC) guidelines to recommend lactate normalization as part of initial resuscitation efforts, particularly when Scv02 is not available.[21] Lactate measurement may assist in recognition of cases of severe sepsis or septic shock and provide valuable triage information, as serum lactate has been shown to predict mortality from severe sepsis independent of shock or organ failure.[22] In a retrospective study of patients presenting to the ED with sepsis, a lactate >4 mmol/L was associated with progression to septic shock within 4 to 48 hours.[23]

Our understanding of the specific benefits of EGDT is far from complete, as 3 recent large prospective, multicenter, randomized trials ProCESS (Protocolized Care for Early Septic Shock), ARISE (Australasian Resuscitation In Sepsis Evaluation), and ProMISe (Protocolised Management in Sepsis) did not show EGDT protocols to be superior to usual care.[24, 25, 26] Interpreted collectively, the benefit of EGDT may not be from targeting specific physiologic parameters, but rather from the early recognition of sepsis and the appropriate use of well‐supported interventions like aggressive fluid resuscitation and early/efficacious antibiotics.[27]

Although the precise benefit of EGDT as a package versus its individual components remains in question, we have a decade of experience in delivering this care as an integral component of the bundles put forth in the SSC guidelines.[28] Observational and retrospective studies have shown increased compliance with guidelines and improved mortality after implementing these protocols, although early bundles for severe sepsis included therapies that have subsequently been called into question on an individual basis like drotrecogin alfa (activated) and glucocorticoid therapy.[29, 30, 31] The mortality benefit from sepsis bundles deserves further explanation, although education and early recognition are likely contributory.[32]

Several studies evaluated individual components of EGDT. The TRISS (Transfusion Requirements in Septic Shock) trial randomized ICU patients with septic shock to 2 different red blood cell transfusion strategies, and found no mortality benefit or reduction in ischemic events for patients transfused at a hemoglobin of 9 g/dL compared to the 7 g/dL threshold.[33] The SEPSISPAM (Assessment of Two Levels of Arterial Pressure on Survival in Patients With Septic Shock) trial compared the MAP goal of 65 to 70 mm Hg to 80 to 85 mm Hg for patients with septic shock in a randomized, multicenter trial.[34] Although there was no difference in 28‐day mortality, more atrial fibrillation was diagnosed in the higher target group. For patients with chronic hypertension, targeting the higher MAP led to less renal injury and reduced the need for renal‐replacement therapy.[34, 35] Identifying specific subsets of patients with sepsis who benefit most from particular therapies should help clinicians set patient‐specific goals and targets.

Although we can expect additional studies to provide further guidance, it is reasonable at present to adhere to protocols designed to improve timely sepsis detection and management with aggressive volume resuscitation, early/efficacious antibiotic administration, and effective infection source control.

ANTIBIOTICS AND SOURCE CONTROL

Administration of broad‐spectrum antibiotics has long been the cornerstone of sepsis management. Timely antibiotic infusion is an integral part of the 2004 and 2012 SSC guidelines,[17, 21] with the caveat that blood cultures should be obtained prior to antibiotic therapy provided that no significant delay (>45 minutes) occurs.[21] Recent studies have begun to address fundamental clinical questions, including the timing of antibiotic administration and the efficacy of empiric antibiotic choice. A landmark retrospective cohort study of ICU patients with septic shock demonstrated survival to hospital discharge was highest in patients who received antibiotics within the first hour of hypotension.[36] Survival decreased on average by 7.6% with each hour that antibiotics were delayed. Only 50% of patients with septic shock in this study received effective antibiotic therapy within 6 hours of documented hypotension.[36] A subsequent retrospective, single‐center cohort study of ED patients with severe sepsis or septic shock undergoing EGDT showed a mortality benefit when antibiotics were administered within the first hour. However, it did not demonstrate a statistically significant decline in survival on an hourly basis thereafter.[37]

A prospective, multicenter ED trial that included patients with severe sepsis in addition to septic shock[38] did not show a mortality benefit to administration of antibiotics within the first hour. In‐hospital mortality risk for patients undergoing EGDT was similar across patients in whom time to antibiotics was delayed up to 6 hours after triage.[36, 38] However, patients with severe sepsis in whom antibiotics were delayed until shock was recognized faced a statistically significant increased risk of death (odds ratio = 2.35; 95% confidence interval = 1.12‐4.53).[38, 39] A retrospective study of 28,150 patients from the SSC database demonstrated a statistically significant increase in mortality for each hour that empiric antibiotics were delayed.[40] Importantly, this trend was preserved regardless of location of sepsis diagnosis (ED, ICU, and hospital ward) and across illness severity. Though there remains debate about the critical importance of the golden hour for antibiotic administration, overall current evidence supports early empiric antibiotics in severe sepsis and septic shock.

Choosing an empiric antibiotic regimen, based on infection source and host factors, also plays a key role in sepsis outcomes. A retrospective study of patients with septic shock from 1996 to 2005 showed that inappropriate initial antibiotics (based on eventual in vitro culture sensitivities or evaluation of clinical syndrome) were used 20% of the time and resulted in a 5‐fold reduction in survival.[41] A retrospective cohort study of patients with gram‐negative bacteremia and severe sepsis or septic shock found prior antibiotic exposure within 90 days to be an independent risk factor for drug resistance and in‐hospital mortality.[42] However, careful consideration of side effects should also influence choice of initial antibiotic therapy. A Cochrane review citing 69 trials and containing 7863 subjects with sepsis compared empiric ‐lactam therapy to ‐lactamaminoglycoside combination therapy.[43] All‐cause mortality and clinical failure was similar in both groups, as was the rate of resistance. Importantly, nephrotoxicity was significantly less in the ‐lactam monotherapy group.[43]

Infection source control is an essential component of sepsis management that should occur simultaneously with antibiotic administration. The 2012 SSC guidelines promote infection source control within 12 hours of diagnosis, with consideration of the risks and benefits therein and preference for interventions with the lowest associated physiologic insult.[21] Intravascular access devices should be recognized as a common source of infection, and should be removed after alternative access has been established.[21]

FLUID RESUSCITATION

Volume resuscitation is an essential component of sepsis management, regardless of algorithm or endpoint. Three main types of nonblood product fluid resuscitation have been used: crystalloid (saline and Ringer's solutions), colloid (typically an albumin‐containing solution), and synthetic volume expanders (hydroxyethyl starch [HES] and similar compounds).

Multiple large studies confirmed the lack of a favorable riskbenefit ratio with synthetic volume expanders. Among nearly 800 patients with severe sepsis who were randomized to receive either Ringer's acetate or HES 130/0.4, a significantly higher number of patients receiving HES died (51% vs 43%, relative risk [RR] = 1.17), and required renal‐replacement therapy (22% vs 16%, RR = 1.35). One patient in each group was dialysis dependent at 90 days.[44] An additional multicenter, prospective study of HES versus 0.9% (normal) saline for fluid resuscitation in the ICU found no significant difference in mortality (18% vs 17%, P = 0.26), but did note a higher need for renal‐replacement therapy in the HES group (7.0% vs 5.8%, RR = 1.21).[45] A systematic review incorporating 9 trials that randomized approximately 3400 patients with sepsis receiving either HES, crystalloid, or colloid showed no difference in mortality, although there was an excess risk for renal‐replacement therapy (RR = 1.36), serious adverse events (RR = 1.30), and red blood cell transfusion (RR = 1.29) in patients receiving HES.[46] A second, larger systematic review concluded that HES was associated with an increased mortality compared with crystalloids, albumin, or gelatin (RR = 1.09). Additionally, an increase in renal failure (RR = 1.27) and renal‐replacement therapy (RR = 1.32) was also noted.[47]

The debate between crystalloid and colloid (namely albumin) for fluid resuscitation is ongoing, with recent important additions to the literature. The SAFE (Saline Versus Albumin Fluid Evaluation) study investigators in 2004 randomized nearly 7000 patients to receive either 4% albumin solution or normal saline. At 28 days, no significant differences were found in mortality, new organ failure, ICU and hospital length of stay, days of mechanical ventilation, or days of renal‐replacement therapy.[48] In 2014, another multicenter prospective study of 1800 patients with severe sepsis or septic shock in 100 ICUs in Italy compared 20% albumin and crystalloid solution to crystalloid solution alone. Mortality, end‐organ dysfunction, and ICU length of stay did not differ between groups.[49] Two 2014 systematic reviews and meta‐analyses on fluid resuscitation produced somewhat differing conclusions. Patel et al. evaluated data from 16 randomized trials including more than 4000 patients receiving albumin for volume resuscitation in adults with sepsis. Albumin provided no significant survival advantage in total or in any subgroup, regardless of severity of illness or baseline albumin level, thus arguing against its routine use.[50] Rochwerg et al. evaluated 14 studies with approximately 19,000 patients using Bayesian network meta‐analysis technique. This study concluded that albumin is associated with reduced mortality compared with other fluids, and also that balanced crystalloids (eg, Ringer's lactate and similar) may have lower mortality than normal saline.[51] A chloride‐restrictive resuscitation approach has also been associated with a lower incidence of acute kidney injury in critically ill adults.[52]

The SSC confirmed its recommendations of a minimum of 30 mL/kg of crystalloids as the initial fluid of choice in sepsis in 2012, but added a suggestion for the addition of albumin in patients requiring substantial amounts of crystalloid.[21] The currently available data suggest crystalloid fluids to be the best‐supported initial fluid in the management of sepsis, and that synthetic colloids should be avoided. Prospective data are still required to answer questions regarding the potential advantages of albumin or balanced and/or chloride‐restricted crystalloids.

ICU CONSIDERATIONS

Appropriate management of patients with the syndrome of sepsis, severe sepsis, and septic shock on the hospital ward requires a working knowledge of recent research conducted in the ICU setting. Although conclusions based on data from patients with septic shock might not be generalizable to less severe cases of sepsis, recent trials on glucose control and corticosteroids deserve consideration.

Intensive insulin treatment in the medical ICU is no longer standard practice. In the NICE‐SUGAR (Normoglycaemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation) trial, a large, multicenter randomized controlled trial of ICU patients, close to 20% of patients had severe sepsis at the time of randomization.[53] This subgroup did not benefit from intensive glucose control (a target of 81108 mg/dL) in terms of 90‐day mortality.[53] In contrast to prior studies of glycemic control in the critically ill, the intensive treatment group overall suffered increased mortality.[54] The COIITSS (Combination of Corticotherapy and Intensive Insulin Therapy for Septic Shock) trial looked at intensive insulin therapy in patients with septic shock being treated with corticosteroids, a group particularly at risk for hyperglycemia. In this study, intensive insulin therapy did not improve in‐hospital mortality.[55] Based on these and other ICU data, the current SSC recommendation is to target a blood glucose of 180 mg/dL for patients with severe sepsis.[21, 56]

The use of corticosteroids to treat the host response in septic shock has been re‐evaluated.[57] The 2004 SSC guidelines recommended hydrocortisone therapy for 7 days in patients with septic shock requiring vasopressor support after fluid resuscitation.[17] This recommendation was based on data from a placebo‐controlled multicenter trial in France that showed improved shock reversal and reduced mortality in patients with septic shock who were treated with hydrocortisone and fludricortisone.[58] Of note, these patients were enrolled on the basis of hypotension despite intravenous fluids and the initiation of 1 vasopressor. The benefit of corticosteroids was seen only in patients deemed to have relative adrenal insufficiency based on response corticotropin testing.[58] However, the CORTICUS (Corticosteroid Therapy of Septic Shock) study, a subsequent multicenter, placebo‐controlled, randomized controlled trial failed to show a benefit to corticotropin testing in identifying patients with septic shock who would benefit from corticorsteroids.[59] The corticosteroid treatment arm similarly benefited from faster shock reversal, but at the expense of increased superinfection.[59] Although underpowered, CORTICUS did not show a survival benefit to corticosteroids in septic shock.[59] The most recent SSC guidelines do not recommend corticotropin (adrenocorticotropic hormone) stimulation testing and do not advise corticosteroids in septic shock if fluid resuscitation and vasopressor therapy restore hemodynamic stability during initial resuscitation.[21] Future studies may clarify subpopulations of patients with sepsis who benefit from corticosteroids.

OUTCOMES: MORTALITY AND COMPLICATIONS

An understanding of the currently available information regarding the morbidity and mortality associated with severe sepsis is essential for the practicing hospitalist. Whether transferring care of patients to or receiving patients from the ICU, hospitalists must lead discussions with patients and families regarding prognosis, especially as it informs disposition. Hospitalists are often asked to make projections on outcome as well as the timing and venue of disposition. Clarification of patient wishes and goals of care remains an essential first step in the care of septic patients. Recently published studies provide prognostic information, including mortality (both short and long term) as well as complications associated with severe sepsis.

The attributable mortality for severe sepsis has been predominantly reported to date as short‐term (usually in‐hospital). A meta‐analysis of US patients from 1991 to 2009 demonstrated a 3% annual decline in the short‐term (28 day) mortality from severe sepsis using 2 previously validated algorithms. Data from 36 trials (and approximately 14,000 patients) revealed a decrease in mortality from 47% in the period from 1991 to 1995 to 29% from 2006 to 2009.[60] Although the methods employed (sepsis definitions and ICD‐9‐CM codes) can have a significant impact on estimates of mortality, these results corroborate a progressive decline in short‐term mortality from severe sepsis in the United States between 2004 and 2009 using 4 validated algorithms.[8] Outside the United States, a recent retrospective analysis of more than 1 million patients with severe sepsis treated in the ICU in Australia and New Zealand from 2000 to 2012 also demonstrated a decrease in adjusted in‐hospital mortality. In this study, short‐term mortality declined yearly, with an odds ratio of death of 0.49 in 2012 compared with 2000.[61] Hospital case volume has also been shown to impact rates of inpatient death, with higher‐volume centers demonstrating lower mortality attributed to severe sepsis.[62, 63]

The sufficiency of short‐term mortality as the sole metric for severe sepsis outcome has been more recently questioned.[64, 65] The extent to which full recovery and significant morbidity are affected relative to the change in death rate is unknown, and as such, more data on morbidity and longer‐term mortality are necessary. A Danish study examined data from several registries of patients with severe sepsis. Compared with community‐matched controls, patients with severe sepsis had an increased risk of death at 30 days (hazard ratio [HR] = 90.8), from 30 days to 1 year (HR = 2.7), and 1 to 4 years (HR = 2.3) after discharge.[66] Older survivors of severe sepsis also appear to have higher healthcare utilization in the year following discharge. An analysis of older severe sepsis survivors showed a striking increase in healthcare use relative to their prior resource use, driven primarily by higher number of days in inpatient healthcare facilities. Survivors of severe sepsis also had a significantly higher 90‐day and 1‐year mortality than matched controls.[67]

Increased attention is currently being given to sepsis‐related complications, especially functional and cognitive impairments in older patients. Sepsis survivorship is a swiftly mounting public health issue for older Americans.[68] An 8‐year follow‐up of older sepsis survivors demonstrated a significant increase in the odds of both physical and cognitive dysfunction. During this period, moderate‐to‐severe cognitive dysfunction increased 3‐fold (6.1% before sepsis, 16.7% after).[69] The mechanism by which this dysfunction occurs is unknown, as are the relative contributions of infection site/etiology, ICU length of stay, and extent of organ dysfunction. New functional impairment has been demonstrated in patients with severe sepsis initially admitted to a general floor, even with good baseline function,[12] as well as decreased quality of life in sepsis survivors.[65, 70] Another study showed more admissions complicated by severe sepsis resulted in discharge to a long‐term care facility in 2007 compared to 2000.[7]

Additional organ‐specific consequences of severe sepsis have also been recently suggested. A retrospective analysis showed an increase in the incidence of new‐onset atrial fibrillation in severe sepsis, with an associated increase in risk of in‐hospital stroke and death. New‐onset atrial fibrillation was present in 5.9% of patients with severe sepsis, compared with 0.65% in patients without. Severe sepsis patients with new‐onset atrial fibrillation had an increased risk of in‐hospital stroke (adjusted odds ratio = 2.70) and mortality (adjusted RR = 1.07).[71] These findings suggest association only, and further investigation is warranted. It remains to be seen whether interventions to restore sinus rhythm or anticoagulation are warranted. Preoperative sepsis (within 48 hours) has also been proposed as a risk for postoperative (30 day) arterial (myocardial infarction, stroke) and venous (deep venous thrombosis, pulmonary embolism) thromboembolism. The authors of this study suggest deferral of elective surgery or specific attention to postoperative thromboprophylaxis in patients in whom procedures must occur.[72] This has particular relevance for those septic patients in whom surgical source control is indicated.

Estimates regarding mortality and specific complications attributable to severe sepsis are ongoing, though clearly with a new focus upon metrics other than short‐term mortality. Furthermore, recent data to suggest source of infection as a major driver of mortality in septic shock[73] may contribute to the evolution of the conceptualization of sepsis similar to that of cancer: a heterogeneous collection of disease, among which mortality is determined by specific subtypes. At present, this much appears clear: the previously held notion that survival of a septic insult is unlikely to have future implications is under siege.[74] The extent to which complications and increased longer‐term mortality may reflect generally poorer health at the time of infection versus a sequelae of the survived episode itself is not yet known.

CONCLUSIONS

The past decade of sepsis research has led to significant findings that will change clinical practice for hospital medicine practitioners. Although the incidence of severe sepsis in the United States has continued to rise, in‐hospital mortality has declined; in this context, the management of the spectrum of sepsis disorders is no longer restricted to the ICU, and the entity of sepsis survivorship has blossomed. Prompt recognition of sepsis and improvements in supportive care are likely responsible for improved patient outcomes. EGDT has been called into question as a protocol whose benefit lies not in specific targets or endpoints, but rather in the early recognition of sepsis, appropriate fluid resuscitation, and early/effective antibiotics. Synthetic volume expanders, intensive insulin therapy, and routine use of corticosteroids are no longer recommended.

Hospitalists are a critical link in providing timely, evidence‐based care for patients with sepsis from initial recognition to post‐ICU recovery. Specialized care for the survivors of septic shock is a burgeoning area, and hospitalists are integral in the management of the sequelae of multiorgan failure.

Disclosure: Nothing to report.

Sepsis is one of the oldest and most elusive syndromes in medicine, and remains a significant contributor to morbidity, mortality, and healthcare expenditure.[1] A 1992 American College of Chest Physicians and Society of Critical Care Medicine consensus conference statement introduced the systemic inflammatory response syndrome (SIRS) into the medical lexicon, along with definitions of sepsis, severe sepsis, and septic shock.[2] A 2003 consensus panel expanded the list of signs and symptoms associated with sepsis, and warned that the findings of SIRS do not differentiate sepsis from other noninfectious conditions.[3] The terminology is important, as these definitions resulted in a shift of the label of the syndrome of infection complicated by end‐organ dysfunction from sepsis to severe sepsis or septic shock. Overlap of these terms has implications for categorizing such infections for the purpose of investigation, estimating epidemiology and outcome, and coding, billing, and reimbursement.[1]

Traditional definitions of the spectrum of sepsis disorders are outlined in Table 1,[2, 3] and it is important to note that an update to these definitions is anticipated in the near future. A recent publication has called into question the sensitivity and categorical requirement of at least 2 SIRS criteria to define severe sepsis.[4] This study of more than 1 million patients from 172 intensive care units (ICUs) in Australia and New Zealand from 2000 to 2013 found that the cutoff of 2 SIRS criteria to define severe sepsis excluded 1 in 8 patients with infection and end‐organ hypoperfusion. SIRS‐negative severe sepsis patients experienced the same mortality as SIRS‐positive patients. In addition, adjusted analysis determined a stepwise increase in mortality risk associated with each additional SIRS criterion without a transition point in risk noted at 2.[4]

Traditional Definitions of Sepsis Spectrum Disorders
Definition

  • NOTE: Abbreviations: SIRS, systemic inflammatory response syndrome.

SIRS The systemic inflammatory response to a variety of severe insults. Requires 2 of the following:
Temperature >38C or 36C
Heart rate >90 beats/minute
Respiratory rate >20 breaths/minute or partial pressure of carbon dioxide (PaCO2) 32 mm Hg
White blood cell count >12,000 or 4,000 cells/L or 10% immature (band) forms
Sepsis The systemic response to infection, with SIRS criteria met in the setting of documented or strongly suspected infection
Severe sepsis Sepsis associated with organ dysfunction, hypoperfusion (including but not limited to lactic acidosis, oliguria, or acute alteration in mental status), or hypotension (systolic blood pressure 90 mm Hg or >40 mm Hg below baseline).
Septic shock Sepsis‐induced hypotension despite adequate volume resuscitation (2030 mL/kg) with perfusion abnormalities including but not limited to lactic acidosis, oliguria, or acute alteration in mental status

From 1979 through 2000, there were over 10 million reported cases of sepsis, which accounted for 1.3% of all hospitalizations in the United States.[5] Normalized to the population distribution of the 2000 US Census, there was an annualized increase in sepsis cases of 8.7%. A 2011 report revealed rates of hospitalization for patients with septicemia or sepsis in the United States more than doubled from 2000 through 2008.[6] Patients with sepsis experienced longer length of stay than other inpatients and were 8 times more likely to die during hospitalization.[6] Estimates of severe sepsis incidence are complicated by how acute organ dysfunction is defined and whether it is related to infection. As of 2001, the number of severe sepsis cases in the United States was believed to exceed 750,000 and comprise approximately 10% of ICU admissions.[1] The incidence of severe sepsis cases in the United States continues to rise.[7, 8, 9] However, a more than doubling of the use of sepsis International Classification of Diseases, Ninth Revision, Clinical Modification (ICD‐9‐CM) codes from 2004 through 2009 has also been noted.[8] Based on ICD‐9‐CM codes indicating the presence of sepsis and organ system failure, the number of severe sepsis hospitalizations per 100,000 persons in the United States increased from 143 in 2000 to 343 in 2007.[7] Total hospital costs for patients with severe sepsis were estimated to increase 57%, from $15.4 billion in 2003 to $24.3 billion in 2007.[9] The Agency for Healthcare Research and Quality considered septicemia the most expensive medical condition in the United States in a 2011 data brief, with annual aggregate hospital costs exceeding $20 billion.[10]

Although many hospitalists care for patients in the ICU and other higher acuity or step‐down units, a significant proportion of patients with severe sepsis receive care on a general medical floor.[11, 12, 13] Sepsis is also clearly not an issue restricted to patients on internal medicine services. Of over 360,000 general surgery patients from 2005 to 2007, the incidences of sepsis (2.3%) and septic shock (1.6%) greatly exceeded those of pulmonary embolism (0.3%) and myocardial infarction (0.2%). In this cohort, the need for emergency surgery and the presence of any comorbidity increased the number of sepsis cases.[14]

Despite difficulties obtaining exact estimates of case numbers, the following appears true: the spectrum of sepsis disorders (including severe sepsis and septic shock) remains a common, costly, and increasing clinical entity that is encountered by hospital medicine physicians in a variety inpatient settings. This review will provide an update for hospitalists based on many important studies that have been published since the last review of this topic in this journal.[15] The expanding evidence base in sepsis includes early goal‐directed therapy (EGDT), clinical endpoints, and bundles of care for sepsis; antibiotics (choice and timing); volume resuscitation; ICU considerations, including the use of insulin and corticosteroids; and mortality, complications, and the advent of the condition of sepsis survivorship.

EARLY GOAL‐DIRECTED THERAPY

A 2001 prospective, randomized trial of EGDT initiated in the emergency department (ED) for patients with severe sepsis and septic shock resulted in an impressive 16% reduction of in‐hospital mortality compared to standard therapy.[16] The intervention protocol included central venous catheter placement and a 500‐mL bolus of crystalloid every 30 minutes to establish a central venous pressure (CVP) of 8 to 12 mm Hg. Vasopressors were used to maintain a mean arterial pressure (MAP) greater than 65 mm Hg, and patients with a MAP greater than 90 mm Hg were given vasodilators. Patients with a central venous oxygen saturation (Scv02) of less than 70% received red blood cell transfusion with a goal hematocrit of 30%. If central venous oxygen saturation remained less than 70% despite these interventions, dobutamine was used for inotropic effect until this goal was achieved or was limited by tachycardia or hypotension.[16]

These results prompted inclusion of the specific hemodynamic targets (CVP, MAP, and Scv02) into the original 2004 Surviving Sepsis Campaign guidelines and spurred a decade of interest worldwide.[17] The incremental importance of these individual components in managing severe sepsis and septic shock has since come under scrutiny. A recent randomized trial suggested that EGDT guided by venous lactate clearance of >10% was noninferior to the goal Scv02 of >70%. However, only 10% of the study population required transfusion or dobutamine.[18, 19] Prospective ICU data on lactate‐guided therapy[20] supported the revised 2012 Surviving Sepsis Campaign (SSC) guidelines to recommend lactate normalization as part of initial resuscitation efforts, particularly when Scv02 is not available.[21] Lactate measurement may assist in recognition of cases of severe sepsis or septic shock and provide valuable triage information, as serum lactate has been shown to predict mortality from severe sepsis independent of shock or organ failure.[22] In a retrospective study of patients presenting to the ED with sepsis, a lactate >4 mmol/L was associated with progression to septic shock within 4 to 48 hours.[23]

Our understanding of the specific benefits of EGDT is far from complete, as 3 recent large prospective, multicenter, randomized trials ProCESS (Protocolized Care for Early Septic Shock), ARISE (Australasian Resuscitation In Sepsis Evaluation), and ProMISe (Protocolised Management in Sepsis) did not show EGDT protocols to be superior to usual care.[24, 25, 26] Interpreted collectively, the benefit of EGDT may not be from targeting specific physiologic parameters, but rather from the early recognition of sepsis and the appropriate use of well‐supported interventions like aggressive fluid resuscitation and early/efficacious antibiotics.[27]

Although the precise benefit of EGDT as a package versus its individual components remains in question, we have a decade of experience in delivering this care as an integral component of the bundles put forth in the SSC guidelines.[28] Observational and retrospective studies have shown increased compliance with guidelines and improved mortality after implementing these protocols, although early bundles for severe sepsis included therapies that have subsequently been called into question on an individual basis like drotrecogin alfa (activated) and glucocorticoid therapy.[29, 30, 31] The mortality benefit from sepsis bundles deserves further explanation, although education and early recognition are likely contributory.[32]

Several studies evaluated individual components of EGDT. The TRISS (Transfusion Requirements in Septic Shock) trial randomized ICU patients with septic shock to 2 different red blood cell transfusion strategies, and found no mortality benefit or reduction in ischemic events for patients transfused at a hemoglobin of 9 g/dL compared to the 7 g/dL threshold.[33] The SEPSISPAM (Assessment of Two Levels of Arterial Pressure on Survival in Patients With Septic Shock) trial compared the MAP goal of 65 to 70 mm Hg to 80 to 85 mm Hg for patients with septic shock in a randomized, multicenter trial.[34] Although there was no difference in 28‐day mortality, more atrial fibrillation was diagnosed in the higher target group. For patients with chronic hypertension, targeting the higher MAP led to less renal injury and reduced the need for renal‐replacement therapy.[34, 35] Identifying specific subsets of patients with sepsis who benefit most from particular therapies should help clinicians set patient‐specific goals and targets.

Although we can expect additional studies to provide further guidance, it is reasonable at present to adhere to protocols designed to improve timely sepsis detection and management with aggressive volume resuscitation, early/efficacious antibiotic administration, and effective infection source control.

ANTIBIOTICS AND SOURCE CONTROL

Administration of broad‐spectrum antibiotics has long been the cornerstone of sepsis management. Timely antibiotic infusion is an integral part of the 2004 and 2012 SSC guidelines,[17, 21] with the caveat that blood cultures should be obtained prior to antibiotic therapy provided that no significant delay (>45 minutes) occurs.[21] Recent studies have begun to address fundamental clinical questions, including the timing of antibiotic administration and the efficacy of empiric antibiotic choice. A landmark retrospective cohort study of ICU patients with septic shock demonstrated survival to hospital discharge was highest in patients who received antibiotics within the first hour of hypotension.[36] Survival decreased on average by 7.6% with each hour that antibiotics were delayed. Only 50% of patients with septic shock in this study received effective antibiotic therapy within 6 hours of documented hypotension.[36] A subsequent retrospective, single‐center cohort study of ED patients with severe sepsis or septic shock undergoing EGDT showed a mortality benefit when antibiotics were administered within the first hour. However, it did not demonstrate a statistically significant decline in survival on an hourly basis thereafter.[37]

A prospective, multicenter ED trial that included patients with severe sepsis in addition to septic shock[38] did not show a mortality benefit to administration of antibiotics within the first hour. In‐hospital mortality risk for patients undergoing EGDT was similar across patients in whom time to antibiotics was delayed up to 6 hours after triage.[36, 38] However, patients with severe sepsis in whom antibiotics were delayed until shock was recognized faced a statistically significant increased risk of death (odds ratio = 2.35; 95% confidence interval = 1.12‐4.53).[38, 39] A retrospective study of 28,150 patients from the SSC database demonstrated a statistically significant increase in mortality for each hour that empiric antibiotics were delayed.[40] Importantly, this trend was preserved regardless of location of sepsis diagnosis (ED, ICU, and hospital ward) and across illness severity. Though there remains debate about the critical importance of the golden hour for antibiotic administration, overall current evidence supports early empiric antibiotics in severe sepsis and septic shock.

Choosing an empiric antibiotic regimen, based on infection source and host factors, also plays a key role in sepsis outcomes. A retrospective study of patients with septic shock from 1996 to 2005 showed that inappropriate initial antibiotics (based on eventual in vitro culture sensitivities or evaluation of clinical syndrome) were used 20% of the time and resulted in a 5‐fold reduction in survival.[41] A retrospective cohort study of patients with gram‐negative bacteremia and severe sepsis or septic shock found prior antibiotic exposure within 90 days to be an independent risk factor for drug resistance and in‐hospital mortality.[42] However, careful consideration of side effects should also influence choice of initial antibiotic therapy. A Cochrane review citing 69 trials and containing 7863 subjects with sepsis compared empiric ‐lactam therapy to ‐lactamaminoglycoside combination therapy.[43] All‐cause mortality and clinical failure was similar in both groups, as was the rate of resistance. Importantly, nephrotoxicity was significantly less in the ‐lactam monotherapy group.[43]

Infection source control is an essential component of sepsis management that should occur simultaneously with antibiotic administration. The 2012 SSC guidelines promote infection source control within 12 hours of diagnosis, with consideration of the risks and benefits therein and preference for interventions with the lowest associated physiologic insult.[21] Intravascular access devices should be recognized as a common source of infection, and should be removed after alternative access has been established.[21]

FLUID RESUSCITATION

Volume resuscitation is an essential component of sepsis management, regardless of algorithm or endpoint. Three main types of nonblood product fluid resuscitation have been used: crystalloid (saline and Ringer's solutions), colloid (typically an albumin‐containing solution), and synthetic volume expanders (hydroxyethyl starch [HES] and similar compounds).

Multiple large studies confirmed the lack of a favorable riskbenefit ratio with synthetic volume expanders. Among nearly 800 patients with severe sepsis who were randomized to receive either Ringer's acetate or HES 130/0.4, a significantly higher number of patients receiving HES died (51% vs 43%, relative risk [RR] = 1.17), and required renal‐replacement therapy (22% vs 16%, RR = 1.35). One patient in each group was dialysis dependent at 90 days.[44] An additional multicenter, prospective study of HES versus 0.9% (normal) saline for fluid resuscitation in the ICU found no significant difference in mortality (18% vs 17%, P = 0.26), but did note a higher need for renal‐replacement therapy in the HES group (7.0% vs 5.8%, RR = 1.21).[45] A systematic review incorporating 9 trials that randomized approximately 3400 patients with sepsis receiving either HES, crystalloid, or colloid showed no difference in mortality, although there was an excess risk for renal‐replacement therapy (RR = 1.36), serious adverse events (RR = 1.30), and red blood cell transfusion (RR = 1.29) in patients receiving HES.[46] A second, larger systematic review concluded that HES was associated with an increased mortality compared with crystalloids, albumin, or gelatin (RR = 1.09). Additionally, an increase in renal failure (RR = 1.27) and renal‐replacement therapy (RR = 1.32) was also noted.[47]

The debate between crystalloid and colloid (namely albumin) for fluid resuscitation is ongoing, with recent important additions to the literature. The SAFE (Saline Versus Albumin Fluid Evaluation) study investigators in 2004 randomized nearly 7000 patients to receive either 4% albumin solution or normal saline. At 28 days, no significant differences were found in mortality, new organ failure, ICU and hospital length of stay, days of mechanical ventilation, or days of renal‐replacement therapy.[48] In 2014, another multicenter prospective study of 1800 patients with severe sepsis or septic shock in 100 ICUs in Italy compared 20% albumin and crystalloid solution to crystalloid solution alone. Mortality, end‐organ dysfunction, and ICU length of stay did not differ between groups.[49] Two 2014 systematic reviews and meta‐analyses on fluid resuscitation produced somewhat differing conclusions. Patel et al. evaluated data from 16 randomized trials including more than 4000 patients receiving albumin for volume resuscitation in adults with sepsis. Albumin provided no significant survival advantage in total or in any subgroup, regardless of severity of illness or baseline albumin level, thus arguing against its routine use.[50] Rochwerg et al. evaluated 14 studies with approximately 19,000 patients using Bayesian network meta‐analysis technique. This study concluded that albumin is associated with reduced mortality compared with other fluids, and also that balanced crystalloids (eg, Ringer's lactate and similar) may have lower mortality than normal saline.[51] A chloride‐restrictive resuscitation approach has also been associated with a lower incidence of acute kidney injury in critically ill adults.[52]

The SSC confirmed its recommendations of a minimum of 30 mL/kg of crystalloids as the initial fluid of choice in sepsis in 2012, but added a suggestion for the addition of albumin in patients requiring substantial amounts of crystalloid.[21] The currently available data suggest crystalloid fluids to be the best‐supported initial fluid in the management of sepsis, and that synthetic colloids should be avoided. Prospective data are still required to answer questions regarding the potential advantages of albumin or balanced and/or chloride‐restricted crystalloids.

ICU CONSIDERATIONS

Appropriate management of patients with the syndrome of sepsis, severe sepsis, and septic shock on the hospital ward requires a working knowledge of recent research conducted in the ICU setting. Although conclusions based on data from patients with septic shock might not be generalizable to less severe cases of sepsis, recent trials on glucose control and corticosteroids deserve consideration.

Intensive insulin treatment in the medical ICU is no longer standard practice. In the NICE‐SUGAR (Normoglycaemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation) trial, a large, multicenter randomized controlled trial of ICU patients, close to 20% of patients had severe sepsis at the time of randomization.[53] This subgroup did not benefit from intensive glucose control (a target of 81108 mg/dL) in terms of 90‐day mortality.[53] In contrast to prior studies of glycemic control in the critically ill, the intensive treatment group overall suffered increased mortality.[54] The COIITSS (Combination of Corticotherapy and Intensive Insulin Therapy for Septic Shock) trial looked at intensive insulin therapy in patients with septic shock being treated with corticosteroids, a group particularly at risk for hyperglycemia. In this study, intensive insulin therapy did not improve in‐hospital mortality.[55] Based on these and other ICU data, the current SSC recommendation is to target a blood glucose of 180 mg/dL for patients with severe sepsis.[21, 56]

The use of corticosteroids to treat the host response in septic shock has been re‐evaluated.[57] The 2004 SSC guidelines recommended hydrocortisone therapy for 7 days in patients with septic shock requiring vasopressor support after fluid resuscitation.[17] This recommendation was based on data from a placebo‐controlled multicenter trial in France that showed improved shock reversal and reduced mortality in patients with septic shock who were treated with hydrocortisone and fludricortisone.[58] Of note, these patients were enrolled on the basis of hypotension despite intravenous fluids and the initiation of 1 vasopressor. The benefit of corticosteroids was seen only in patients deemed to have relative adrenal insufficiency based on response corticotropin testing.[58] However, the CORTICUS (Corticosteroid Therapy of Septic Shock) study, a subsequent multicenter, placebo‐controlled, randomized controlled trial failed to show a benefit to corticotropin testing in identifying patients with septic shock who would benefit from corticorsteroids.[59] The corticosteroid treatment arm similarly benefited from faster shock reversal, but at the expense of increased superinfection.[59] Although underpowered, CORTICUS did not show a survival benefit to corticosteroids in septic shock.[59] The most recent SSC guidelines do not recommend corticotropin (adrenocorticotropic hormone) stimulation testing and do not advise corticosteroids in septic shock if fluid resuscitation and vasopressor therapy restore hemodynamic stability during initial resuscitation.[21] Future studies may clarify subpopulations of patients with sepsis who benefit from corticosteroids.

OUTCOMES: MORTALITY AND COMPLICATIONS

An understanding of the currently available information regarding the morbidity and mortality associated with severe sepsis is essential for the practicing hospitalist. Whether transferring care of patients to or receiving patients from the ICU, hospitalists must lead discussions with patients and families regarding prognosis, especially as it informs disposition. Hospitalists are often asked to make projections on outcome as well as the timing and venue of disposition. Clarification of patient wishes and goals of care remains an essential first step in the care of septic patients. Recently published studies provide prognostic information, including mortality (both short and long term) as well as complications associated with severe sepsis.

The attributable mortality for severe sepsis has been predominantly reported to date as short‐term (usually in‐hospital). A meta‐analysis of US patients from 1991 to 2009 demonstrated a 3% annual decline in the short‐term (28 day) mortality from severe sepsis using 2 previously validated algorithms. Data from 36 trials (and approximately 14,000 patients) revealed a decrease in mortality from 47% in the period from 1991 to 1995 to 29% from 2006 to 2009.[60] Although the methods employed (sepsis definitions and ICD‐9‐CM codes) can have a significant impact on estimates of mortality, these results corroborate a progressive decline in short‐term mortality from severe sepsis in the United States between 2004 and 2009 using 4 validated algorithms.[8] Outside the United States, a recent retrospective analysis of more than 1 million patients with severe sepsis treated in the ICU in Australia and New Zealand from 2000 to 2012 also demonstrated a decrease in adjusted in‐hospital mortality. In this study, short‐term mortality declined yearly, with an odds ratio of death of 0.49 in 2012 compared with 2000.[61] Hospital case volume has also been shown to impact rates of inpatient death, with higher‐volume centers demonstrating lower mortality attributed to severe sepsis.[62, 63]

The sufficiency of short‐term mortality as the sole metric for severe sepsis outcome has been more recently questioned.[64, 65] The extent to which full recovery and significant morbidity are affected relative to the change in death rate is unknown, and as such, more data on morbidity and longer‐term mortality are necessary. A Danish study examined data from several registries of patients with severe sepsis. Compared with community‐matched controls, patients with severe sepsis had an increased risk of death at 30 days (hazard ratio [HR] = 90.8), from 30 days to 1 year (HR = 2.7), and 1 to 4 years (HR = 2.3) after discharge.[66] Older survivors of severe sepsis also appear to have higher healthcare utilization in the year following discharge. An analysis of older severe sepsis survivors showed a striking increase in healthcare use relative to their prior resource use, driven primarily by higher number of days in inpatient healthcare facilities. Survivors of severe sepsis also had a significantly higher 90‐day and 1‐year mortality than matched controls.[67]

Increased attention is currently being given to sepsis‐related complications, especially functional and cognitive impairments in older patients. Sepsis survivorship is a swiftly mounting public health issue for older Americans.[68] An 8‐year follow‐up of older sepsis survivors demonstrated a significant increase in the odds of both physical and cognitive dysfunction. During this period, moderate‐to‐severe cognitive dysfunction increased 3‐fold (6.1% before sepsis, 16.7% after).[69] The mechanism by which this dysfunction occurs is unknown, as are the relative contributions of infection site/etiology, ICU length of stay, and extent of organ dysfunction. New functional impairment has been demonstrated in patients with severe sepsis initially admitted to a general floor, even with good baseline function,[12] as well as decreased quality of life in sepsis survivors.[65, 70] Another study showed more admissions complicated by severe sepsis resulted in discharge to a long‐term care facility in 2007 compared to 2000.[7]

Additional organ‐specific consequences of severe sepsis have also been recently suggested. A retrospective analysis showed an increase in the incidence of new‐onset atrial fibrillation in severe sepsis, with an associated increase in risk of in‐hospital stroke and death. New‐onset atrial fibrillation was present in 5.9% of patients with severe sepsis, compared with 0.65% in patients without. Severe sepsis patients with new‐onset atrial fibrillation had an increased risk of in‐hospital stroke (adjusted odds ratio = 2.70) and mortality (adjusted RR = 1.07).[71] These findings suggest association only, and further investigation is warranted. It remains to be seen whether interventions to restore sinus rhythm or anticoagulation are warranted. Preoperative sepsis (within 48 hours) has also been proposed as a risk for postoperative (30 day) arterial (myocardial infarction, stroke) and venous (deep venous thrombosis, pulmonary embolism) thromboembolism. The authors of this study suggest deferral of elective surgery or specific attention to postoperative thromboprophylaxis in patients in whom procedures must occur.[72] This has particular relevance for those septic patients in whom surgical source control is indicated.

Estimates regarding mortality and specific complications attributable to severe sepsis are ongoing, though clearly with a new focus upon metrics other than short‐term mortality. Furthermore, recent data to suggest source of infection as a major driver of mortality in septic shock[73] may contribute to the evolution of the conceptualization of sepsis similar to that of cancer: a heterogeneous collection of disease, among which mortality is determined by specific subtypes. At present, this much appears clear: the previously held notion that survival of a septic insult is unlikely to have future implications is under siege.[74] The extent to which complications and increased longer‐term mortality may reflect generally poorer health at the time of infection versus a sequelae of the survived episode itself is not yet known.

CONCLUSIONS

The past decade of sepsis research has led to significant findings that will change clinical practice for hospital medicine practitioners. Although the incidence of severe sepsis in the United States has continued to rise, in‐hospital mortality has declined; in this context, the management of the spectrum of sepsis disorders is no longer restricted to the ICU, and the entity of sepsis survivorship has blossomed. Prompt recognition of sepsis and improvements in supportive care are likely responsible for improved patient outcomes. EGDT has been called into question as a protocol whose benefit lies not in specific targets or endpoints, but rather in the early recognition of sepsis, appropriate fluid resuscitation, and early/effective antibiotics. Synthetic volume expanders, intensive insulin therapy, and routine use of corticosteroids are no longer recommended.

Hospitalists are a critical link in providing timely, evidence‐based care for patients with sepsis from initial recognition to post‐ICU recovery. Specialized care for the survivors of septic shock is a burgeoning area, and hospitalists are integral in the management of the sequelae of multiorgan failure.

Disclosure: Nothing to report.

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  42. Johnson MT, Reichley R, Hoppe‐Bauer J, Dunne WM, Micek S, Kollef M. Impact of previous antibiotic therapy on outcome of gram‐negative severe sepsis. Crit Care Med. 2011;39(8):1859–1865.
  43. Paul M, Lador A, Grozinsky‐Glasberg S, Leibovici L. Beta lactam antibiotic monotherapy versus beta lactam‐aminoglycoside antibiotic combination therapy for sepsis. Cochrane Database Syst Rev. 2014;1:CD003344.
  44. Perner A, Haase N, Guttormsen AB, et al. Hydroxyethyl starch 130/0.42 versus ringer's acetate in severe sepsis. N Engl J Med. 2012;367(2):124–134.
  45. Myburgh JA, Finfer S, Bellomo R, et al.; CHEST Investigators; Australian and New Zealand Intensive Care Society Clinical Trials Group. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med. 2012;367(20):1901–1911.
  46. Haase N, Perner A, Hennings LI, et al. Hydroxyethyl starch 130/0.38–0.45 versus crystalloid or albumin in patients with sepsis: systematic review with meta‐analysis and trial sequential analysis. BMJ. 2013;346:f839.
  47. Zarychanski R, Abou‐Setta AM, Turgeon AF, et al. Association of hydroxyethyl starch administration with mortality and acute kidney injury in critically ill patients requiring volume resuscitation: a systematic review and meta‐analysis. JAMA. 2013;309(7):678–688.
  48. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R; SAFE Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350(22):2247–2256.
  49. Caironi P, Tognoni G, Masson S, et al. Albumin replacement in patients with severe sepsis or septic shock. N Engl J Med. 2014;370(15):1412–1421.
  50. Patel A, Laffan MA, Waheed U, Brett SJ. Randomised trials of human albumin for adults with sepsis: systematic review and meta‐analysis with trial sequential analysis of all‐cause mortality. BMJ. 2014;349:g4561.
  51. Rochwerg B, Alhazzani W, Sindi A, et al. Fluid resuscitation in sepsis: a systematic review and network meta‐analysis. Ann Intern Med. 2014;161(5):347–355.
  52. Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M. Association between a chloride‐liberal vs chloride‐restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA. 2012;308(15):1566–1572.
  53. NICE‐SUGAR Study Investigators, Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283–1297.
  54. Inzucchi SE, Siegel MD. Glucose control in the ICU—how tight is too tight? N Engl J Med. 2009;360(13):1346–1349.
  55. COIITSS Study Investigators, Annane D, Cariou A, Maxime V, et al. Corticosteroid treatment and intensive insulin therapy for septic shock in adults: a randomized controlled trial. JAMA. 2010;303(4):341–348.
  56. Griesdale DE, Souza RJ, Dam RM, et al. Intensive insulin therapy and mortality among critically ill patients: a meta‐analysis including NICE‐SUGAR study data. CMAJ. 2009;180(8):821–827.
  57. Annane D, Bellissant E, Bollaert PE, et al. Corticosteroids in the treatment of severe sepsis and septic shock in adults: a systematic review. JAMA. 2009;301(22):2362–2375.
  58. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002;288(7):862–871.
  59. Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008;358(2):111–124.
  60. Stevenson EK, Rubenstein AR, Radin GT, Wiener RS, Walkey AJ. Two decades of mortality trends among patients with severe sepsis: a comparative meta‐analysis. Crit Care Med. 2014;42(3):625–631.
  61. Kaukonen KM, Bailey M, Suzuki S, Pilcher D, Bellomo R. Mortality related to severe sepsis and septic shock among critically ill patients in Australia and New Zealand, 2000–2012. JAMA. 2014;311(13):1308–1316.
  62. Gaieski DF, Edwards M, Kallan MJ, Mikkelsen ME, Goyal M, Carr BG. The relationship between hospital volume and mortality in severe sepsis. Am J Respir Crit Care Med. 2014;190(6):665–674.
  63. Walkey AJ, Wiener RS. Hospital case volume and outcomes among patients hospitalized with severe sepsis. Am J Respir Crit Care Med. 2014;189(5):548–555.
  64. Iwashyna TJ, Angus DC. Declining case fatality rates for severe sepsis: Good data bring good news with ambiguous implications. JAMA. 2014;311(13):1295–1297.
  65. Winters BD, Eberlein M, Leung J, Needham DM, Pronovost PJ, Sevransky JE. Long‐term mortality and quality of life in sepsis: a systematic review. Crit Care Med. 2010;38(5):1276–1283.
  66. Storgaard M, Hallas J, Gahrn‐Hansen B, Pedersen SS, Pedersen C, Lassen AT. Short‐ and long‐term mortality in patients with community‐acquired severe sepsis and septic shock. Scand J Infect Dis. 2013;45(8):577–583.
  67. Prescott HC, Langa KM, Liu V, Escobar GJ, Iwashyna TJ. Increased 1‐year healthcare use in survivors of severe sepsis. Am J Respir Crit Care Med. 2014;190(1):62–69.
  68. Iwashyna TJ, Cooke CR, Wunsch H, Kahn JM. Population burden of long‐term survivorship after severe sepsis in older Americans. J Am Geriatr Soc. 2012;60(6):1070–1077.
  69. Iwashyna TJ, Ely EW, Smith DM, Langa KM. Long‐term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787–1794.
  70. Karlsson S, Ruokonen E, Varpula T, Ala‐Kokko TI, Pettilä V; Finnsepsis Study Group. Long‐term outcome and quality‐adjusted life years after severe sepsis. Crit Care Med. 2009;37(4):1268–1274.
  71. Walkey AJ, Wiener RS, Ghobrial JM, Curtis LH, Benjamin EJ. Incident stroke and mortality associated with new‐onset atrial fibrillation in patients hospitalized with severe sepsis. JAMA. 2011;306(20):2248–2254.
  72. Donze JD, Ridker PM, Finlayson SR, Bates DW. Impact of sepsis on risk of postoperative arterial and venous thromboses: large prospective cohort study. BMJ. 2014;349:g5334.
  73. Leligdowicz A, Dodek PM, Norena M, Wong H, Kumar A, Kumar A; Co‐operative Antimicrobial Therapy of Septic Shock Database Research Group. Association between source of infection and hospital mortality in patients who have septic shock. Am J Respir Crit Care Med. 2014;189(10):1204–1213.
  74. Angus DC. The lingering consequences of sepsis: a hidden public health disaster? JAMA. 2010;304(16):1833–1834.
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  30. Miller RR, Dong L, Nelson NC, et al. Multicenter implementation of a severe sepsis and septic shock treatment bundle. Am J Respir Crit Care Med. 2013;188(1):77–82.
  31. Cannon CM, Holthaus CV, Zubrow MT, et al. The GENESIS project (Generalized early sepsis intervention strategies): a multicenter quality improvement collaborative. J Intensive Care Med. 2013;28(6):355–368.
  32. Ramar K, Gajic O. Early recognition and treatment of severe sepsis. Am J Respir Crit Care Med. 2013;188(1):7–8.
  33. Holst LB, Haase N, Wetterslev J, et al. Lower versus higher hemoglobin threshold for transfusion in septic shock. N Engl J Med. 2014;371(15):1381–1391.
  34. Asfar P, Meziani F, Hamel JF, et al. High versus low blood‐pressure target in patients with septic shock. N Engl J Med. 2014;370(17):1583–1593.
  35. Russell JA. Is there a good MAP for septic shock? N Engl J Med. 2014;370(17):1649–1651.
  36. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006;34(6):1589–1596.
  37. Gaieski DF, Mikkelsen ME, Band RA, et al. Impact of time to antibiotics on survival in patients with severe sepsis or septic shock in whom early goal‐directed therapy was initiated in the emergency department. Crit Care Med. 2010;38(4):1045–1053.
  38. Puskarich MA, Trzeciak S, Shapiro NI, et al. Association between timing of antibiotic administration and mortality from septic shock in patients treated with a quantitative resuscitation protocol. Crit Care Med. 2011;39(9):2066–2071.
  39. Mikkelsen ME, Gaieski DF. Antibiotics in sepsis: timing, appropriateness, and (of course) timely recognition of appropriateness. Crit Care Med. 2011;39(9):2184–2186.
  40. Ferrer R, Martin‐Loeches I, Phillips G, et al. Empiric antibiotic treatment reduces mortality in severe sepsis and septic shock from the first hour: results from a guideline‐based performance improvement program. Crit Care Med. 2014;42(8):1749–1755.
  41. Kumar A, Ellis P, Arabi Y, et al. Initiation of inappropriate antimicrobial therapy results in a fivefold reduction of survival in human septic shock. Chest. 2009;136(5):1237–1248.
  42. Johnson MT, Reichley R, Hoppe‐Bauer J, Dunne WM, Micek S, Kollef M. Impact of previous antibiotic therapy on outcome of gram‐negative severe sepsis. Crit Care Med. 2011;39(8):1859–1865.
  43. Paul M, Lador A, Grozinsky‐Glasberg S, Leibovici L. Beta lactam antibiotic monotherapy versus beta lactam‐aminoglycoside antibiotic combination therapy for sepsis. Cochrane Database Syst Rev. 2014;1:CD003344.
  44. Perner A, Haase N, Guttormsen AB, et al. Hydroxyethyl starch 130/0.42 versus ringer's acetate in severe sepsis. N Engl J Med. 2012;367(2):124–134.
  45. Myburgh JA, Finfer S, Bellomo R, et al.; CHEST Investigators; Australian and New Zealand Intensive Care Society Clinical Trials Group. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med. 2012;367(20):1901–1911.
  46. Haase N, Perner A, Hennings LI, et al. Hydroxyethyl starch 130/0.38–0.45 versus crystalloid or albumin in patients with sepsis: systematic review with meta‐analysis and trial sequential analysis. BMJ. 2013;346:f839.
  47. Zarychanski R, Abou‐Setta AM, Turgeon AF, et al. Association of hydroxyethyl starch administration with mortality and acute kidney injury in critically ill patients requiring volume resuscitation: a systematic review and meta‐analysis. JAMA. 2013;309(7):678–688.
  48. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R; SAFE Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350(22):2247–2256.
  49. Caironi P, Tognoni G, Masson S, et al. Albumin replacement in patients with severe sepsis or septic shock. N Engl J Med. 2014;370(15):1412–1421.
  50. Patel A, Laffan MA, Waheed U, Brett SJ. Randomised trials of human albumin for adults with sepsis: systematic review and meta‐analysis with trial sequential analysis of all‐cause mortality. BMJ. 2014;349:g4561.
  51. Rochwerg B, Alhazzani W, Sindi A, et al. Fluid resuscitation in sepsis: a systematic review and network meta‐analysis. Ann Intern Med. 2014;161(5):347–355.
  52. Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M. Association between a chloride‐liberal vs chloride‐restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA. 2012;308(15):1566–1572.
  53. NICE‐SUGAR Study Investigators, Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283–1297.
  54. Inzucchi SE, Siegel MD. Glucose control in the ICU—how tight is too tight? N Engl J Med. 2009;360(13):1346–1349.
  55. COIITSS Study Investigators, Annane D, Cariou A, Maxime V, et al. Corticosteroid treatment and intensive insulin therapy for septic shock in adults: a randomized controlled trial. JAMA. 2010;303(4):341–348.
  56. Griesdale DE, Souza RJ, Dam RM, et al. Intensive insulin therapy and mortality among critically ill patients: a meta‐analysis including NICE‐SUGAR study data. CMAJ. 2009;180(8):821–827.
  57. Annane D, Bellissant E, Bollaert PE, et al. Corticosteroids in the treatment of severe sepsis and septic shock in adults: a systematic review. JAMA. 2009;301(22):2362–2375.
  58. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002;288(7):862–871.
  59. Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008;358(2):111–124.
  60. Stevenson EK, Rubenstein AR, Radin GT, Wiener RS, Walkey AJ. Two decades of mortality trends among patients with severe sepsis: a comparative meta‐analysis. Crit Care Med. 2014;42(3):625–631.
  61. Kaukonen KM, Bailey M, Suzuki S, Pilcher D, Bellomo R. Mortality related to severe sepsis and septic shock among critically ill patients in Australia and New Zealand, 2000–2012. JAMA. 2014;311(13):1308–1316.
  62. Gaieski DF, Edwards M, Kallan MJ, Mikkelsen ME, Goyal M, Carr BG. The relationship between hospital volume and mortality in severe sepsis. Am J Respir Crit Care Med. 2014;190(6):665–674.
  63. Walkey AJ, Wiener RS. Hospital case volume and outcomes among patients hospitalized with severe sepsis. Am J Respir Crit Care Med. 2014;189(5):548–555.
  64. Iwashyna TJ, Angus DC. Declining case fatality rates for severe sepsis: Good data bring good news with ambiguous implications. JAMA. 2014;311(13):1295–1297.
  65. Winters BD, Eberlein M, Leung J, Needham DM, Pronovost PJ, Sevransky JE. Long‐term mortality and quality of life in sepsis: a systematic review. Crit Care Med. 2010;38(5):1276–1283.
  66. Storgaard M, Hallas J, Gahrn‐Hansen B, Pedersen SS, Pedersen C, Lassen AT. Short‐ and long‐term mortality in patients with community‐acquired severe sepsis and septic shock. Scand J Infect Dis. 2013;45(8):577–583.
  67. Prescott HC, Langa KM, Liu V, Escobar GJ, Iwashyna TJ. Increased 1‐year healthcare use in survivors of severe sepsis. Am J Respir Crit Care Med. 2014;190(1):62–69.
  68. Iwashyna TJ, Cooke CR, Wunsch H, Kahn JM. Population burden of long‐term survivorship after severe sepsis in older Americans. J Am Geriatr Soc. 2012;60(6):1070–1077.
  69. Iwashyna TJ, Ely EW, Smith DM, Langa KM. Long‐term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787–1794.
  70. Karlsson S, Ruokonen E, Varpula T, Ala‐Kokko TI, Pettilä V; Finnsepsis Study Group. Long‐term outcome and quality‐adjusted life years after severe sepsis. Crit Care Med. 2009;37(4):1268–1274.
  71. Walkey AJ, Wiener RS, Ghobrial JM, Curtis LH, Benjamin EJ. Incident stroke and mortality associated with new‐onset atrial fibrillation in patients hospitalized with severe sepsis. JAMA. 2011;306(20):2248–2254.
  72. Donze JD, Ridker PM, Finlayson SR, Bates DW. Impact of sepsis on risk of postoperative arterial and venous thromboses: large prospective cohort study. BMJ. 2014;349:g5334.
  73. Leligdowicz A, Dodek PM, Norena M, Wong H, Kumar A, Kumar A; Co‐operative Antimicrobial Therapy of Septic Shock Database Research Group. Association between source of infection and hospital mortality in patients who have septic shock. Am J Respir Crit Care Med. 2014;189(10):1204–1213.
  74. Angus DC. The lingering consequences of sepsis: a hidden public health disaster? JAMA. 2010;304(16):1833–1834.
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Sepsis: An update in management
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Was the ObGyn’s dexterity compromised?

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Was the ObGyn’s dexterity compromised?

Was the ObGyn’s dexterity compromised?
A woman underwent a hysterectomy. During surgery, the patient’s bladder was injured; the ObGyn called in a urologist to make the repair. 

Patient’s claim The ObGyn failed to inform the patient about the possible complications from hysterectomy. The patient also claimed fraudulent concealment because the ObGyn had suffered a serious injury 3 years earlier that affected his dexterity. At the time of surgery, the ObGyn had a pending lawsuit against the owner of the premises where he fell in which he claimed that he was unable to continue his surgical practice because of the injury. The ObGyn never informed the patient of the extent of his injury or any associated risks related to his injury.

Defendants’ defense The patient was fully informed that bladder injury is a known risk of the procedure. The ObGyn maintained that his injury only affected his ability to stand for many hours while operating. The hospital settled during trial.

Verdict A $12,000 Louisiana settlement was reached with the hospital. Summary judgment was granted to the ObGyn on the informed consent claim. A $30,000 verdict was returned on the fraud count.

 

Placental abruption: Was child dead?
At 32 weeks’ gestation, a woman was found to have placental abruption. At the hospital, her ObGyn could not find a fetal heartbeat or detectable fetal movement on ultrasonography. A radiologist performed another ultrasound 30 minutes later and detected a fetal heart rate of 47 bpm. An emergency cesarean delivery was performed. Soon after birth, the child had seizures and was found to have hypoxic ischemic encephalopathy and diffuse brain injury. The child is profoundly disabled. 

Parents’ claim The ObGyn was negligent for failing to detect the fetal heart rate and in failing to respond properly to placental abruption. Cesarean delivery should have been performed immediately after placental abruption was identified.

Defendant’s defense The case was settled at trial.

Verdict A $13 million Illinois settlement was reached, including $5 million in cash and $8 million placed in trust for the child.

 

Large fetus, shoulder dystocia: Erb’s palsy
Labor was induced at 39 weeks’ gestation because the fetus was anticipated to be large. During vaginal delivery, shoulder dystocia was encountered. At birth, the baby weighed 9 lb 2 oz. She sustained a brachial plexus injury to the posterior shoulder with permanent nerve root damage and Erb’s palsy. The child continues to have limited use of her left arm and hand even after 3 corrective operations.  

Parents’ claim While performing maneuvers to relieve shoulder dystocia, the ObGyn exerted excessive traction on the baby’s head, causing a C-5 nerve root injury and complete avulsion at C-8. A cesarean delivery should have been performed.

Physician’s defense There was no negligence. The nerve injury was caused by the natural forces of labor and the mother’s pushing while the posterior shoulder was wedged behind the mother’s sa-
cral promontory.

Verdict A $1 million Illinois verdict was returned.  

 

Woman dies from toxemia
A 22-year-old woman was seen by her ObGyn 4 days after vaginal delivery. Early the next day, the patient had a seizure at home and was transported by ambulance to the hospital. She could not be resuscitated and died. At autopsy, the cause of death was determined to be toxemia from pregnancy. 

Estate’s claim The ObGyn failed to properly diagnose and treat the patient’s hypertension.

Defendant’s defense The case was settled during trial.

Verdict A $775,000 New York settlement was reached.

 

Blood transfusion delayed for hours: $14.75M net award
After emergency cesarean delivery, the baby was extremely anemic. The physicians determined that a fetal-maternal hemorrhage had started days before, causing the fetus to lose most of her blood.

An hour after birth, the attending neonatologist ordered blood from the hospital’s blood bank and arranged for emergency transport to a neonatal intensive care unit (NICU). Blood transfusion did not occur prior to transport. The child has severe cerebral palsy (CP) and cannot walk or talk at age 8 years.

Parents’ claim The neonatologist ordered cross-matched blood, which, because it is tested for compatibility, takes longer to supply. Universal donor blood could have been delivered in 20 minutes or less because it is readily available. The ambulance from the receiving hospital took an hour to drive 9 miles between the facilities, a trip that should have taken 12 minutes. The ambulance staff did not call ahead to the medical center to have blood ready for the baby. It took 4.5 hours before the newborn received a blood transfusion, a delay that caused severe injury to the child.

 

 

Defendants’ defense The matter went to trial against the neonatologist and his employer after the other defendants settled. 

Verdict Before trial, an ObGyn and the hospital settled for a combined $750,000, and the county agreed to a $12 million settlement. During trial, a $2 million Illinois settlement was reached.

 

Pregnant woman has a massive stroke: $10.9M
Pregnant with her third child and at 26 weeks’ gestation, a 35-year-old woman had a massive intracerebral hemorrhage at home.

The day before, she had contacted her ObGyn’s office to report severe headache and abdominal pain. The call was taken by an associate of her ObGyn, who told her there was no need to go to the hospital and suggested that she had a gastrointestinal virus.

The stroke caused severe cognitive impairment, loss of memory, partial vision loss, dysphasia, and partial paralysis on her right side. At trial, she was still undergoing therapy to regain mobility, speech, and memory. She uses a wheelchair. 

Patient’s claim The covering ObGyn was negligent for not sending the patient to the hospital when she reported severe headache.

Defendants’ defense The ObGyn and medical practice denied negligence, contending that the patient’s pregnancy was normal and that there was no indication that she was at risk for a stroke.

Verdict A $10,928,188 Ohio verdict was returned.

 

Was the fetus properly monitored?
One month before her due date, a woman was found to have premature rupture of membranes. She had gestational diabetes controlled by diet. She was admitted for induction of labor.

For more than 12 hours, external fetal monitor heart-rate tracings were reassuring. Then tracings began to show variable decelerations. For a period of 90 minutes, it was impossible to evaluate the fetal heart rate because the monitor was not working. An internal monitor was not placed. Just prior to birth, the tracings showed a 15-minute period of fetal tachycardia with the heart rate at 180 bpm. The physician’s notes indicated that the baby’s head had crowned for a prolonged period of time.

The baby was floppy at birth with Apgar scores of 2, 4, and 6 at 1, 5, and 10 minutes, respectively. The child was resuscitated and transferred to the NICU. She was found to have perinatal asphyxia, severe metabolic acidosis, multiorgan injury, hypoxic ischemic encephalopathy, and seizures. She stayed in the NICU for 1 month. At age 9 years, she has developmental delays and memory problems, but no motor injuries. 

Parents’ claim During the 90 minutes in which the fetal heart-rate monitor was not working properly, the fetus was in distress. An emergency cesarean delivery should have been performed when variable decelerations were seen on tracings.

Physician’s defense The lack of motor injury indicates that the injury was not related to birth.

Verdict A $2 million Michigan settlement was reached.

 

Rectal tear after vacuum extraction
Vacuum extraction was used to deliver a 47-year-old woman’s child. Later, the mother developed a rectovaginal fistula that became inflamed and involved vaginal passage of stool. The patient required 2 operations and still has residual complications.

Patient’s claim The ObGyn should have found and repaired the rectal tear at delivery. Vacuum extraction was used after only 2 pushes. The mother did not consent to the use of the vacuum extractor.

Physician’s defense The ObGyn admitted that he did not specifically remember this delivery. He claimed that there was informed consent and that the rectal injury was small and easy to overlook.

Verdict A $1.02 million New York verdict was returned.

 

Preeclamptic mother dies after giving birth
A 24-year-old woman developed preeclampsia when under prenatal care at a hospital clinic. At 36 weeks’ gestation, she presented to the clinic with a headache, “seeing spots,” and feeling ill; her blood pressure (BP) was 169/89 mm Hg. She was admitted for induction of labor and treated for preeclampsia with magnesium sulfate. A healthy baby was born 2 days later. The mother continued to have high BP and was prescribed nifedipine.

Her BP was 148/88 mm Hg at discharge. No antihypertensive medications were prescribed. She was given standard postpartum instructions and told to schedule a follow-up appointment in 6 to 8 weeks.

Five days after discharge, she experienced shortness of breath and swelling in her extremities, but did not seek medical attention until the next day, when breathing became labored. When emergency medical services arrived, she was in cardiac arrest. Prolonged resuscitation was required with intubation and artificial respiration. A computed tomo­g-raphy (CT) scan revealed cerebral edema from prolonged hypoxia. She was transferred to another hospital where a neurologist determined that she had suffered a profound anoxic brain injury. She died 3 days later.

 

 

Estate’s claim The hospital staff was negligent for failing to inform the patient of the signs and symptoms of continuing preeclampsia and for not prescribing antihypertensive medication at discharge. Her follow-up appointment should have been scheduled for 1 week.

Defendant’s defense The patient was given oral instructions regarding postpartum preeclampsia. The case was settled during trial.

Verdict A $50,000 North Carolina settlement was reached.

 

Was delivery properly managed?
When a 16-year-old woman was found to have preeclampsia, she was admitted and labor was induced using oxytocin. An external fetal heart-rate monitor was placed.

Three hours later, her ObGyn took over her care from the attending physician. He saw the patient once in the evening, then left to deliver a baby at another hospital. He maintained telephone contact with labor and delivery nurses, who told him that the mother’s labor was progressing as planned. Early the next morning, the nurse called the ObGyn to report that the mother was fully dilated and ready to deliver. The ObGyn was at the patient’s bedside within 30 minutes. After the mother pushed once, the ObGyn determined that a cesarean delivery was necessary.

After birth, the child suffered seizures in the NICU and was transferred to another facility. With CP and microcephaly, he cannot speak, is incontinent, has motor difficulties, and will require 24-hour care for life. 

Parent’s claim Labor was not properly monitored. Oxytocin doses were too large and continued for too long.

Defendants’ defense The mother’s treatment was appropriate and timely. There was no negligence.

Verdict A confidential Kansas settlement was reached with another defendant during the trial. A defense verdict was returned for the ObGyn.

 

Evidence of CMV on ultrasonography
During her pregnancy in 2012, a woman contracted congenital cytomegalovirus (CMV), although she did not have any symptoms. The child has CP, a hearing deficiency, and other complications caused by the virus.

Parents’ claim The ObGyn failed to identify CMV, despite ultrasound evidence that the virus was affecting the fetus. Studies available at the time of the pregnancy show considerable success in treating the condition in utero with hyperimmune globulin antiviral agents.

Defendant’s defense The case was settled during trial.

Verdict A confidential Idaho settlement was reached.  

 

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements, & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.


Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

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Stop staring at that Category-II fetal heart-rate tracing…

Was the ObGyn’s dexterity compromised?
A woman underwent a hysterectomy. During surgery, the patient’s bladder was injured; the ObGyn called in a urologist to make the repair. 

Patient’s claim The ObGyn failed to inform the patient about the possible complications from hysterectomy. The patient also claimed fraudulent concealment because the ObGyn had suffered a serious injury 3 years earlier that affected his dexterity. At the time of surgery, the ObGyn had a pending lawsuit against the owner of the premises where he fell in which he claimed that he was unable to continue his surgical practice because of the injury. The ObGyn never informed the patient of the extent of his injury or any associated risks related to his injury.

Defendants’ defense The patient was fully informed that bladder injury is a known risk of the procedure. The ObGyn maintained that his injury only affected his ability to stand for many hours while operating. The hospital settled during trial.

Verdict A $12,000 Louisiana settlement was reached with the hospital. Summary judgment was granted to the ObGyn on the informed consent claim. A $30,000 verdict was returned on the fraud count.

 

Placental abruption: Was child dead?
At 32 weeks’ gestation, a woman was found to have placental abruption. At the hospital, her ObGyn could not find a fetal heartbeat or detectable fetal movement on ultrasonography. A radiologist performed another ultrasound 30 minutes later and detected a fetal heart rate of 47 bpm. An emergency cesarean delivery was performed. Soon after birth, the child had seizures and was found to have hypoxic ischemic encephalopathy and diffuse brain injury. The child is profoundly disabled. 

Parents’ claim The ObGyn was negligent for failing to detect the fetal heart rate and in failing to respond properly to placental abruption. Cesarean delivery should have been performed immediately after placental abruption was identified.

Defendant’s defense The case was settled at trial.

Verdict A $13 million Illinois settlement was reached, including $5 million in cash and $8 million placed in trust for the child.

 

Large fetus, shoulder dystocia: Erb’s palsy
Labor was induced at 39 weeks’ gestation because the fetus was anticipated to be large. During vaginal delivery, shoulder dystocia was encountered. At birth, the baby weighed 9 lb 2 oz. She sustained a brachial plexus injury to the posterior shoulder with permanent nerve root damage and Erb’s palsy. The child continues to have limited use of her left arm and hand even after 3 corrective operations.  

Parents’ claim While performing maneuvers to relieve shoulder dystocia, the ObGyn exerted excessive traction on the baby’s head, causing a C-5 nerve root injury and complete avulsion at C-8. A cesarean delivery should have been performed.

Physician’s defense There was no negligence. The nerve injury was caused by the natural forces of labor and the mother’s pushing while the posterior shoulder was wedged behind the mother’s sa-
cral promontory.

Verdict A $1 million Illinois verdict was returned.  

 

Woman dies from toxemia
A 22-year-old woman was seen by her ObGyn 4 days after vaginal delivery. Early the next day, the patient had a seizure at home and was transported by ambulance to the hospital. She could not be resuscitated and died. At autopsy, the cause of death was determined to be toxemia from pregnancy. 

Estate’s claim The ObGyn failed to properly diagnose and treat the patient’s hypertension.

Defendant’s defense The case was settled during trial.

Verdict A $775,000 New York settlement was reached.

 

Blood transfusion delayed for hours: $14.75M net award
After emergency cesarean delivery, the baby was extremely anemic. The physicians determined that a fetal-maternal hemorrhage had started days before, causing the fetus to lose most of her blood.

An hour after birth, the attending neonatologist ordered blood from the hospital’s blood bank and arranged for emergency transport to a neonatal intensive care unit (NICU). Blood transfusion did not occur prior to transport. The child has severe cerebral palsy (CP) and cannot walk or talk at age 8 years.

Parents’ claim The neonatologist ordered cross-matched blood, which, because it is tested for compatibility, takes longer to supply. Universal donor blood could have been delivered in 20 minutes or less because it is readily available. The ambulance from the receiving hospital took an hour to drive 9 miles between the facilities, a trip that should have taken 12 minutes. The ambulance staff did not call ahead to the medical center to have blood ready for the baby. It took 4.5 hours before the newborn received a blood transfusion, a delay that caused severe injury to the child.

 

 

Defendants’ defense The matter went to trial against the neonatologist and his employer after the other defendants settled. 

Verdict Before trial, an ObGyn and the hospital settled for a combined $750,000, and the county agreed to a $12 million settlement. During trial, a $2 million Illinois settlement was reached.

 

Pregnant woman has a massive stroke: $10.9M
Pregnant with her third child and at 26 weeks’ gestation, a 35-year-old woman had a massive intracerebral hemorrhage at home.

The day before, she had contacted her ObGyn’s office to report severe headache and abdominal pain. The call was taken by an associate of her ObGyn, who told her there was no need to go to the hospital and suggested that she had a gastrointestinal virus.

The stroke caused severe cognitive impairment, loss of memory, partial vision loss, dysphasia, and partial paralysis on her right side. At trial, she was still undergoing therapy to regain mobility, speech, and memory. She uses a wheelchair. 

Patient’s claim The covering ObGyn was negligent for not sending the patient to the hospital when she reported severe headache.

Defendants’ defense The ObGyn and medical practice denied negligence, contending that the patient’s pregnancy was normal and that there was no indication that she was at risk for a stroke.

Verdict A $10,928,188 Ohio verdict was returned.

 

Was the fetus properly monitored?
One month before her due date, a woman was found to have premature rupture of membranes. She had gestational diabetes controlled by diet. She was admitted for induction of labor.

For more than 12 hours, external fetal monitor heart-rate tracings were reassuring. Then tracings began to show variable decelerations. For a period of 90 minutes, it was impossible to evaluate the fetal heart rate because the monitor was not working. An internal monitor was not placed. Just prior to birth, the tracings showed a 15-minute period of fetal tachycardia with the heart rate at 180 bpm. The physician’s notes indicated that the baby’s head had crowned for a prolonged period of time.

The baby was floppy at birth with Apgar scores of 2, 4, and 6 at 1, 5, and 10 minutes, respectively. The child was resuscitated and transferred to the NICU. She was found to have perinatal asphyxia, severe metabolic acidosis, multiorgan injury, hypoxic ischemic encephalopathy, and seizures. She stayed in the NICU for 1 month. At age 9 years, she has developmental delays and memory problems, but no motor injuries. 

Parents’ claim During the 90 minutes in which the fetal heart-rate monitor was not working properly, the fetus was in distress. An emergency cesarean delivery should have been performed when variable decelerations were seen on tracings.

Physician’s defense The lack of motor injury indicates that the injury was not related to birth.

Verdict A $2 million Michigan settlement was reached.

 

Rectal tear after vacuum extraction
Vacuum extraction was used to deliver a 47-year-old woman’s child. Later, the mother developed a rectovaginal fistula that became inflamed and involved vaginal passage of stool. The patient required 2 operations and still has residual complications.

Patient’s claim The ObGyn should have found and repaired the rectal tear at delivery. Vacuum extraction was used after only 2 pushes. The mother did not consent to the use of the vacuum extractor.

Physician’s defense The ObGyn admitted that he did not specifically remember this delivery. He claimed that there was informed consent and that the rectal injury was small and easy to overlook.

Verdict A $1.02 million New York verdict was returned.

 

Preeclamptic mother dies after giving birth
A 24-year-old woman developed preeclampsia when under prenatal care at a hospital clinic. At 36 weeks’ gestation, she presented to the clinic with a headache, “seeing spots,” and feeling ill; her blood pressure (BP) was 169/89 mm Hg. She was admitted for induction of labor and treated for preeclampsia with magnesium sulfate. A healthy baby was born 2 days later. The mother continued to have high BP and was prescribed nifedipine.

Her BP was 148/88 mm Hg at discharge. No antihypertensive medications were prescribed. She was given standard postpartum instructions and told to schedule a follow-up appointment in 6 to 8 weeks.

Five days after discharge, she experienced shortness of breath and swelling in her extremities, but did not seek medical attention until the next day, when breathing became labored. When emergency medical services arrived, she was in cardiac arrest. Prolonged resuscitation was required with intubation and artificial respiration. A computed tomo­g-raphy (CT) scan revealed cerebral edema from prolonged hypoxia. She was transferred to another hospital where a neurologist determined that she had suffered a profound anoxic brain injury. She died 3 days later.

 

 

Estate’s claim The hospital staff was negligent for failing to inform the patient of the signs and symptoms of continuing preeclampsia and for not prescribing antihypertensive medication at discharge. Her follow-up appointment should have been scheduled for 1 week.

Defendant’s defense The patient was given oral instructions regarding postpartum preeclampsia. The case was settled during trial.

Verdict A $50,000 North Carolina settlement was reached.

 

Was delivery properly managed?
When a 16-year-old woman was found to have preeclampsia, she was admitted and labor was induced using oxytocin. An external fetal heart-rate monitor was placed.

Three hours later, her ObGyn took over her care from the attending physician. He saw the patient once in the evening, then left to deliver a baby at another hospital. He maintained telephone contact with labor and delivery nurses, who told him that the mother’s labor was progressing as planned. Early the next morning, the nurse called the ObGyn to report that the mother was fully dilated and ready to deliver. The ObGyn was at the patient’s bedside within 30 minutes. After the mother pushed once, the ObGyn determined that a cesarean delivery was necessary.

After birth, the child suffered seizures in the NICU and was transferred to another facility. With CP and microcephaly, he cannot speak, is incontinent, has motor difficulties, and will require 24-hour care for life. 

Parent’s claim Labor was not properly monitored. Oxytocin doses were too large and continued for too long.

Defendants’ defense The mother’s treatment was appropriate and timely. There was no negligence.

Verdict A confidential Kansas settlement was reached with another defendant during the trial. A defense verdict was returned for the ObGyn.

 

Evidence of CMV on ultrasonography
During her pregnancy in 2012, a woman contracted congenital cytomegalovirus (CMV), although she did not have any symptoms. The child has CP, a hearing deficiency, and other complications caused by the virus.

Parents’ claim The ObGyn failed to identify CMV, despite ultrasound evidence that the virus was affecting the fetus. Studies available at the time of the pregnancy show considerable success in treating the condition in utero with hyperimmune globulin antiviral agents.

Defendant’s defense The case was settled during trial.

Verdict A confidential Idaho settlement was reached.  

 

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements, & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.


Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Was the ObGyn’s dexterity compromised?
A woman underwent a hysterectomy. During surgery, the patient’s bladder was injured; the ObGyn called in a urologist to make the repair. 

Patient’s claim The ObGyn failed to inform the patient about the possible complications from hysterectomy. The patient also claimed fraudulent concealment because the ObGyn had suffered a serious injury 3 years earlier that affected his dexterity. At the time of surgery, the ObGyn had a pending lawsuit against the owner of the premises where he fell in which he claimed that he was unable to continue his surgical practice because of the injury. The ObGyn never informed the patient of the extent of his injury or any associated risks related to his injury.

Defendants’ defense The patient was fully informed that bladder injury is a known risk of the procedure. The ObGyn maintained that his injury only affected his ability to stand for many hours while operating. The hospital settled during trial.

Verdict A $12,000 Louisiana settlement was reached with the hospital. Summary judgment was granted to the ObGyn on the informed consent claim. A $30,000 verdict was returned on the fraud count.

 

Placental abruption: Was child dead?
At 32 weeks’ gestation, a woman was found to have placental abruption. At the hospital, her ObGyn could not find a fetal heartbeat or detectable fetal movement on ultrasonography. A radiologist performed another ultrasound 30 minutes later and detected a fetal heart rate of 47 bpm. An emergency cesarean delivery was performed. Soon after birth, the child had seizures and was found to have hypoxic ischemic encephalopathy and diffuse brain injury. The child is profoundly disabled. 

Parents’ claim The ObGyn was negligent for failing to detect the fetal heart rate and in failing to respond properly to placental abruption. Cesarean delivery should have been performed immediately after placental abruption was identified.

Defendant’s defense The case was settled at trial.

Verdict A $13 million Illinois settlement was reached, including $5 million in cash and $8 million placed in trust for the child.

 

Large fetus, shoulder dystocia: Erb’s palsy
Labor was induced at 39 weeks’ gestation because the fetus was anticipated to be large. During vaginal delivery, shoulder dystocia was encountered. At birth, the baby weighed 9 lb 2 oz. She sustained a brachial plexus injury to the posterior shoulder with permanent nerve root damage and Erb’s palsy. The child continues to have limited use of her left arm and hand even after 3 corrective operations.  

Parents’ claim While performing maneuvers to relieve shoulder dystocia, the ObGyn exerted excessive traction on the baby’s head, causing a C-5 nerve root injury and complete avulsion at C-8. A cesarean delivery should have been performed.

Physician’s defense There was no negligence. The nerve injury was caused by the natural forces of labor and the mother’s pushing while the posterior shoulder was wedged behind the mother’s sa-
cral promontory.

Verdict A $1 million Illinois verdict was returned.  

 

Woman dies from toxemia
A 22-year-old woman was seen by her ObGyn 4 days after vaginal delivery. Early the next day, the patient had a seizure at home and was transported by ambulance to the hospital. She could not be resuscitated and died. At autopsy, the cause of death was determined to be toxemia from pregnancy. 

Estate’s claim The ObGyn failed to properly diagnose and treat the patient’s hypertension.

Defendant’s defense The case was settled during trial.

Verdict A $775,000 New York settlement was reached.

 

Blood transfusion delayed for hours: $14.75M net award
After emergency cesarean delivery, the baby was extremely anemic. The physicians determined that a fetal-maternal hemorrhage had started days before, causing the fetus to lose most of her blood.

An hour after birth, the attending neonatologist ordered blood from the hospital’s blood bank and arranged for emergency transport to a neonatal intensive care unit (NICU). Blood transfusion did not occur prior to transport. The child has severe cerebral palsy (CP) and cannot walk or talk at age 8 years.

Parents’ claim The neonatologist ordered cross-matched blood, which, because it is tested for compatibility, takes longer to supply. Universal donor blood could have been delivered in 20 minutes or less because it is readily available. The ambulance from the receiving hospital took an hour to drive 9 miles between the facilities, a trip that should have taken 12 minutes. The ambulance staff did not call ahead to the medical center to have blood ready for the baby. It took 4.5 hours before the newborn received a blood transfusion, a delay that caused severe injury to the child.

 

 

Defendants’ defense The matter went to trial against the neonatologist and his employer after the other defendants settled. 

Verdict Before trial, an ObGyn and the hospital settled for a combined $750,000, and the county agreed to a $12 million settlement. During trial, a $2 million Illinois settlement was reached.

 

Pregnant woman has a massive stroke: $10.9M
Pregnant with her third child and at 26 weeks’ gestation, a 35-year-old woman had a massive intracerebral hemorrhage at home.

The day before, she had contacted her ObGyn’s office to report severe headache and abdominal pain. The call was taken by an associate of her ObGyn, who told her there was no need to go to the hospital and suggested that she had a gastrointestinal virus.

The stroke caused severe cognitive impairment, loss of memory, partial vision loss, dysphasia, and partial paralysis on her right side. At trial, she was still undergoing therapy to regain mobility, speech, and memory. She uses a wheelchair. 

Patient’s claim The covering ObGyn was negligent for not sending the patient to the hospital when she reported severe headache.

Defendants’ defense The ObGyn and medical practice denied negligence, contending that the patient’s pregnancy was normal and that there was no indication that she was at risk for a stroke.

Verdict A $10,928,188 Ohio verdict was returned.

 

Was the fetus properly monitored?
One month before her due date, a woman was found to have premature rupture of membranes. She had gestational diabetes controlled by diet. She was admitted for induction of labor.

For more than 12 hours, external fetal monitor heart-rate tracings were reassuring. Then tracings began to show variable decelerations. For a period of 90 minutes, it was impossible to evaluate the fetal heart rate because the monitor was not working. An internal monitor was not placed. Just prior to birth, the tracings showed a 15-minute period of fetal tachycardia with the heart rate at 180 bpm. The physician’s notes indicated that the baby’s head had crowned for a prolonged period of time.

The baby was floppy at birth with Apgar scores of 2, 4, and 6 at 1, 5, and 10 minutes, respectively. The child was resuscitated and transferred to the NICU. She was found to have perinatal asphyxia, severe metabolic acidosis, multiorgan injury, hypoxic ischemic encephalopathy, and seizures. She stayed in the NICU for 1 month. At age 9 years, she has developmental delays and memory problems, but no motor injuries. 

Parents’ claim During the 90 minutes in which the fetal heart-rate monitor was not working properly, the fetus was in distress. An emergency cesarean delivery should have been performed when variable decelerations were seen on tracings.

Physician’s defense The lack of motor injury indicates that the injury was not related to birth.

Verdict A $2 million Michigan settlement was reached.

 

Rectal tear after vacuum extraction
Vacuum extraction was used to deliver a 47-year-old woman’s child. Later, the mother developed a rectovaginal fistula that became inflamed and involved vaginal passage of stool. The patient required 2 operations and still has residual complications.

Patient’s claim The ObGyn should have found and repaired the rectal tear at delivery. Vacuum extraction was used after only 2 pushes. The mother did not consent to the use of the vacuum extractor.

Physician’s defense The ObGyn admitted that he did not specifically remember this delivery. He claimed that there was informed consent and that the rectal injury was small and easy to overlook.

Verdict A $1.02 million New York verdict was returned.

 

Preeclamptic mother dies after giving birth
A 24-year-old woman developed preeclampsia when under prenatal care at a hospital clinic. At 36 weeks’ gestation, she presented to the clinic with a headache, “seeing spots,” and feeling ill; her blood pressure (BP) was 169/89 mm Hg. She was admitted for induction of labor and treated for preeclampsia with magnesium sulfate. A healthy baby was born 2 days later. The mother continued to have high BP and was prescribed nifedipine.

Her BP was 148/88 mm Hg at discharge. No antihypertensive medications were prescribed. She was given standard postpartum instructions and told to schedule a follow-up appointment in 6 to 8 weeks.

Five days after discharge, she experienced shortness of breath and swelling in her extremities, but did not seek medical attention until the next day, when breathing became labored. When emergency medical services arrived, she was in cardiac arrest. Prolonged resuscitation was required with intubation and artificial respiration. A computed tomo­g-raphy (CT) scan revealed cerebral edema from prolonged hypoxia. She was transferred to another hospital where a neurologist determined that she had suffered a profound anoxic brain injury. She died 3 days later.

 

 

Estate’s claim The hospital staff was negligent for failing to inform the patient of the signs and symptoms of continuing preeclampsia and for not prescribing antihypertensive medication at discharge. Her follow-up appointment should have been scheduled for 1 week.

Defendant’s defense The patient was given oral instructions regarding postpartum preeclampsia. The case was settled during trial.

Verdict A $50,000 North Carolina settlement was reached.

 

Was delivery properly managed?
When a 16-year-old woman was found to have preeclampsia, she was admitted and labor was induced using oxytocin. An external fetal heart-rate monitor was placed.

Three hours later, her ObGyn took over her care from the attending physician. He saw the patient once in the evening, then left to deliver a baby at another hospital. He maintained telephone contact with labor and delivery nurses, who told him that the mother’s labor was progressing as planned. Early the next morning, the nurse called the ObGyn to report that the mother was fully dilated and ready to deliver. The ObGyn was at the patient’s bedside within 30 minutes. After the mother pushed once, the ObGyn determined that a cesarean delivery was necessary.

After birth, the child suffered seizures in the NICU and was transferred to another facility. With CP and microcephaly, he cannot speak, is incontinent, has motor difficulties, and will require 24-hour care for life. 

Parent’s claim Labor was not properly monitored. Oxytocin doses were too large and continued for too long.

Defendants’ defense The mother’s treatment was appropriate and timely. There was no negligence.

Verdict A confidential Kansas settlement was reached with another defendant during the trial. A defense verdict was returned for the ObGyn.

 

Evidence of CMV on ultrasonography
During her pregnancy in 2012, a woman contracted congenital cytomegalovirus (CMV), although she did not have any symptoms. The child has CP, a hearing deficiency, and other complications caused by the virus.

Parents’ claim The ObGyn failed to identify CMV, despite ultrasound evidence that the virus was affecting the fetus. Studies available at the time of the pregnancy show considerable success in treating the condition in utero with hyperimmune globulin antiviral agents.

Defendant’s defense The case was settled during trial.

Verdict A confidential Idaho settlement was reached.  

 

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements, & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.


Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

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Was the ObGyn’s dexterity compromised?
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Was the ObGyn’s dexterity compromised?
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Medical Verdicts, notable judgments and settlements, Lewis Laska, Medical Malpractice, Medical Malpractice Verdicts Settlements & Experts, hysterectomy, bladder injury, verdict, placental abruption, Erb's palsy, induction of labor, toxemia, blood transfusion, emergency cesarean delivery, neonatologist, ObGyn, intracerebral hemorrhage, stroke, severe headache, fetal heart-rate monitor, rectal tear, vacuum extraction, preeclampsia, blood pressure, hypertension, oxytocin, cytomegalovirus, CMV,
Legacy Keywords
Medical Verdicts, notable judgments and settlements, Lewis Laska, Medical Malpractice, Medical Malpractice Verdicts Settlements & Experts, hysterectomy, bladder injury, verdict, placental abruption, Erb's palsy, induction of labor, toxemia, blood transfusion, emergency cesarean delivery, neonatologist, ObGyn, intracerebral hemorrhage, stroke, severe headache, fetal heart-rate monitor, rectal tear, vacuum extraction, preeclampsia, blood pressure, hypertension, oxytocin, cytomegalovirus, CMV,
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   In this Article

 

  • Placental abruption: Was child dead?
  • Large fetus, shoulder dystocia: Erb’s palsy
  • Woman dies from toxemia
  • Blood transfusion delayed for hours: $14.75M net award
  • Pregnant woman has a massive stroke: $10.9M
  • Was the fetus properly monitored?
  • Rectal tear after vacuum extraction
  • Preeclamptic mother dies after giving birth
  • Was delivery properly managed?
  • Evidence of CMV on ultrasonography
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A survey of liability claims against obstetric providers highlights major areas of contention

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A survey of liability claims against obstetric providers highlights major areas of contention
Author(s)
Janelle Yates
Senior Editor

An analysis of 882 obstetric claims closed between 2007 and 2014 highlighted 3 common allegationsby patients1:

  • a delay in the treatment of fetal distress (22%). The term “fetal distress” remains a common allegation in malpractice claims. Cases in this category most often reflected a delay or failure to act in the face of Category II or III fetal heart-rate tracings.
  • improper performance of vaginal delivery (20%). Almost half of the cases in this category involved brachial plexus injuries linked to shoulder dystocia. Patients alleged that improper maneuvers were used to resolve the dystocia. The remainder of cases in this category involved forceps and vacuum extraction deliveries.
  • improper management of pregnancy (17%). Among the allegations were a failure to test for fetal abnormalities, failure to recognize complications of pregnancy, and failure to address abnormal findings.

Together, these 3 allegations accounted for 59% of claims. Other allegations included diagnosis-related claims, delay in delivery, improper performance of operative delivery, retained foreign bodies, and improper choice of delivery method.1

Where are the really big malpractice awards?

Everything may be bigger in Texas, but New York is the biggest in at least 1 area: large medical malpractice payments. New York had more than 3 times as many $1 million-plus malpractice awards as any other state in 2014, according to data from the National Practitioner Data Bank (NPDB).1

New York physicians had 210 malpractice payments of $1 million or more reported to the NPDB last year, compared with 61 for Illinois, the next-highest state. Rounding out the top 5 were Massachusetts with 49, followed by California with 43, and New Jersey with 41, the NPDB data show.

After taking population into account, New York was still the leader with 10.66 large awards per million residents. Next in this category was the New England trio of Rhode Island, which had 9.42 such payments per 1 million population; Massachusetts (7.26); and Connecticut (6.39).

In 2014, there were 4 states that had no malpractice payments of at least $1 million reported to the NPDB: Alaska, Kansas, North Dakota, and Nebraska, with Kansas having the largest population. In states with at least one $1 million-plus malpractice payment, Texas physicians had the lowest rate per million population, 0.22—just 6 awards from a population of 27 million.

Reference
1. NPDB Research Statistics. National Practitioner Data Bank. http://www.npdb.hrsa.gov/resources/npdbstats/npdbStatistics.jsp. Accessed
July 17, 2015.

Copyright © 2015 Ob.Gyn. News Digital Network, Frontline Medical Communications. Available at: http://www.obgynews.com/?id=11146&tx_ttnews[tt_news]=417377&cHash=5cc8cd69fa7c8a1186aaeec0e814e4e4


The Obstetrics Closed Claims Study findings were released earlier this spring by the Napa, California−based Doctors Company, the nation’s largest physician-owned medical malpractice insurer.1 Susan Mann, MD,a spokesperson for the company, provided expert commentary on the study at the 2015 Annual Clinical Meeting of the American College of Obstetricians and Gynecologists in San Francisco (see “Frequent sources of malpractice claims” below).

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

Frequent sources of malpractice claims
Communication breakdowns and treatment delays are frequent sources of malpractice claims. Susan Mann, MD, spokesperson for The Doctors Company, the nation’s largest physician-owned medical malpractice insurer, discusses the underlying practice vulnerabilities revealed by the Obstetrics Closed Claims Study.
Dr. Mann practices obstetrics and gynecology in Brookline, Massachusetts, and at Beth Israel Deaconess Medical Center in Boston. She is president of the QualBridge Institute, a consulting firm focused on issues of quality and safety.


Top 7 factors contributing to patient injury
The Doctors Company identified specific factors that contributed to patient injury in the closed claims1:  

  1. Selection and management of therapy(34%). Among the issues here were decisions involving augmentation of labor, route of delivery, and the timing of interventions. This factor also related to medications—for example, a failure to order antibiotics for Group A and Group B strep, a failure to order Rho(D) immune globulin for Rh-negative mothers, and a failure to provide magnesium sulfate for women with eclampsia.
  2. Patient-assessment issues (32%). The Doctors Company reviewers found that physicians frequently failed to consider information that was available, or overlooked abnormal findings.
  3. Technical performance (18%). This factor involved problems associated with known risks of various procedures, such as postpartum hemorrhage and brachial plexus injuries. It also included poor technique.
  4. Communication problems among providers (17%).
  5. Patient factors (16%). These factors included a failure to comply with therapy or to show up for appointments.
  6. Insufficient notes or a lack of documentation (14%).
  7. Communication problems between patient/family and provider (14%).

“Studying obstetrical medical malpractice claims sheds light on the wide array of problems that may arise during pregnancy and in labor and delivery,” the study authors conclude. “Many of these cases reflect unusual maternal or neonatal conditions that can be diagnosed only with vigilance. Examples include protein deficiencies, clotting abnormalities, placental abruptions, infections, and genetic abnormalities. More common conditions should be identified with close attention to vital signs, laboratory studies, changes to maternal and neonatal conditions, and patient complaints.”1 See “Tips for reducing malpractice claims in obstetrics” below.

 

 

Tips for reducing malpractice claims in obstetrics1

The Obstetrics Closed Claim Study identified a number of “underlying vulnerabilities” that place patients at risk and increase liability for clinicians. The Doctors Company offers the following tips to help reduce these claims:

Require periodic training and certification for physicians and nurses to maintain competency and facilitate conversations about fetal heart-rate (FHR) tracing interpretation. Both parties should use the same terminology when discussing the strips.

Use technology that allows physicians to review FHR patterns from remote locations so that physicians and nurses are able to see the same information when discussing next steps.

When operative vaginal delivery is attempted in the face of a Category III FHR tracing, a contingency team should be available for possible emergent cesarean delivery.

Foster a culture in which caregivers feel comfortable speaking up if they have a concern. Ensure that the organization has a well-defined escalation guideline.


“Obstetric departments must plan for clinical emergencies by developing and maintaining physician and staff competencies through mock drills and simulations that reduce the likelihood of injuries to mothers and their infants,” the study authors conclude.1

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

References

Reference
1. The Doctors Company. Obstetrics Closed Claim Study. http://www.thedoctors.com/KnowledgeCenter/Pa tient Safety/articles/CON_ID_011803. Published April 2015. Accessed May 6, 2015. 

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An analysis of 882 obstetric claims closed between 2007 and 2014 highlighted 3 common allegationsby patients1:

  • a delay in the treatment of fetal distress (22%). The term “fetal distress” remains a common allegation in malpractice claims. Cases in this category most often reflected a delay or failure to act in the face of Category II or III fetal heart-rate tracings.
  • improper performance of vaginal delivery (20%). Almost half of the cases in this category involved brachial plexus injuries linked to shoulder dystocia. Patients alleged that improper maneuvers were used to resolve the dystocia. The remainder of cases in this category involved forceps and vacuum extraction deliveries.
  • improper management of pregnancy (17%). Among the allegations were a failure to test for fetal abnormalities, failure to recognize complications of pregnancy, and failure to address abnormal findings.

Together, these 3 allegations accounted for 59% of claims. Other allegations included diagnosis-related claims, delay in delivery, improper performance of operative delivery, retained foreign bodies, and improper choice of delivery method.1

Where are the really big malpractice awards?

Everything may be bigger in Texas, but New York is the biggest in at least 1 area: large medical malpractice payments. New York had more than 3 times as many $1 million-plus malpractice awards as any other state in 2014, according to data from the National Practitioner Data Bank (NPDB).1

New York physicians had 210 malpractice payments of $1 million or more reported to the NPDB last year, compared with 61 for Illinois, the next-highest state. Rounding out the top 5 were Massachusetts with 49, followed by California with 43, and New Jersey with 41, the NPDB data show.

After taking population into account, New York was still the leader with 10.66 large awards per million residents. Next in this category was the New England trio of Rhode Island, which had 9.42 such payments per 1 million population; Massachusetts (7.26); and Connecticut (6.39).

In 2014, there were 4 states that had no malpractice payments of at least $1 million reported to the NPDB: Alaska, Kansas, North Dakota, and Nebraska, with Kansas having the largest population. In states with at least one $1 million-plus malpractice payment, Texas physicians had the lowest rate per million population, 0.22—just 6 awards from a population of 27 million.

Reference
1. NPDB Research Statistics. National Practitioner Data Bank. http://www.npdb.hrsa.gov/resources/npdbstats/npdbStatistics.jsp. Accessed
July 17, 2015.

Copyright © 2015 Ob.Gyn. News Digital Network, Frontline Medical Communications. Available at: http://www.obgynews.com/?id=11146&tx_ttnews[tt_news]=417377&cHash=5cc8cd69fa7c8a1186aaeec0e814e4e4


The Obstetrics Closed Claims Study findings were released earlier this spring by the Napa, California−based Doctors Company, the nation’s largest physician-owned medical malpractice insurer.1 Susan Mann, MD,a spokesperson for the company, provided expert commentary on the study at the 2015 Annual Clinical Meeting of the American College of Obstetricians and Gynecologists in San Francisco (see “Frequent sources of malpractice claims” below).

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

Frequent sources of malpractice claims
Communication breakdowns and treatment delays are frequent sources of malpractice claims. Susan Mann, MD, spokesperson for The Doctors Company, the nation’s largest physician-owned medical malpractice insurer, discusses the underlying practice vulnerabilities revealed by the Obstetrics Closed Claims Study.
Dr. Mann practices obstetrics and gynecology in Brookline, Massachusetts, and at Beth Israel Deaconess Medical Center in Boston. She is president of the QualBridge Institute, a consulting firm focused on issues of quality and safety.


Top 7 factors contributing to patient injury
The Doctors Company identified specific factors that contributed to patient injury in the closed claims1:  

  1. Selection and management of therapy(34%). Among the issues here were decisions involving augmentation of labor, route of delivery, and the timing of interventions. This factor also related to medications—for example, a failure to order antibiotics for Group A and Group B strep, a failure to order Rho(D) immune globulin for Rh-negative mothers, and a failure to provide magnesium sulfate for women with eclampsia.
  2. Patient-assessment issues (32%). The Doctors Company reviewers found that physicians frequently failed to consider information that was available, or overlooked abnormal findings.
  3. Technical performance (18%). This factor involved problems associated with known risks of various procedures, such as postpartum hemorrhage and brachial plexus injuries. It also included poor technique.
  4. Communication problems among providers (17%).
  5. Patient factors (16%). These factors included a failure to comply with therapy or to show up for appointments.
  6. Insufficient notes or a lack of documentation (14%).
  7. Communication problems between patient/family and provider (14%).

“Studying obstetrical medical malpractice claims sheds light on the wide array of problems that may arise during pregnancy and in labor and delivery,” the study authors conclude. “Many of these cases reflect unusual maternal or neonatal conditions that can be diagnosed only with vigilance. Examples include protein deficiencies, clotting abnormalities, placental abruptions, infections, and genetic abnormalities. More common conditions should be identified with close attention to vital signs, laboratory studies, changes to maternal and neonatal conditions, and patient complaints.”1 See “Tips for reducing malpractice claims in obstetrics” below.

 

 

Tips for reducing malpractice claims in obstetrics1

The Obstetrics Closed Claim Study identified a number of “underlying vulnerabilities” that place patients at risk and increase liability for clinicians. The Doctors Company offers the following tips to help reduce these claims:

Require periodic training and certification for physicians and nurses to maintain competency and facilitate conversations about fetal heart-rate (FHR) tracing interpretation. Both parties should use the same terminology when discussing the strips.

Use technology that allows physicians to review FHR patterns from remote locations so that physicians and nurses are able to see the same information when discussing next steps.

When operative vaginal delivery is attempted in the face of a Category III FHR tracing, a contingency team should be available for possible emergent cesarean delivery.

Foster a culture in which caregivers feel comfortable speaking up if they have a concern. Ensure that the organization has a well-defined escalation guideline.


“Obstetric departments must plan for clinical emergencies by developing and maintaining physician and staff competencies through mock drills and simulations that reduce the likelihood of injuries to mothers and their infants,” the study authors conclude.1

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

An analysis of 882 obstetric claims closed between 2007 and 2014 highlighted 3 common allegationsby patients1:

  • a delay in the treatment of fetal distress (22%). The term “fetal distress” remains a common allegation in malpractice claims. Cases in this category most often reflected a delay or failure to act in the face of Category II or III fetal heart-rate tracings.
  • improper performance of vaginal delivery (20%). Almost half of the cases in this category involved brachial plexus injuries linked to shoulder dystocia. Patients alleged that improper maneuvers were used to resolve the dystocia. The remainder of cases in this category involved forceps and vacuum extraction deliveries.
  • improper management of pregnancy (17%). Among the allegations were a failure to test for fetal abnormalities, failure to recognize complications of pregnancy, and failure to address abnormal findings.

Together, these 3 allegations accounted for 59% of claims. Other allegations included diagnosis-related claims, delay in delivery, improper performance of operative delivery, retained foreign bodies, and improper choice of delivery method.1

Where are the really big malpractice awards?

Everything may be bigger in Texas, but New York is the biggest in at least 1 area: large medical malpractice payments. New York had more than 3 times as many $1 million-plus malpractice awards as any other state in 2014, according to data from the National Practitioner Data Bank (NPDB).1

New York physicians had 210 malpractice payments of $1 million or more reported to the NPDB last year, compared with 61 for Illinois, the next-highest state. Rounding out the top 5 were Massachusetts with 49, followed by California with 43, and New Jersey with 41, the NPDB data show.

After taking population into account, New York was still the leader with 10.66 large awards per million residents. Next in this category was the New England trio of Rhode Island, which had 9.42 such payments per 1 million population; Massachusetts (7.26); and Connecticut (6.39).

In 2014, there were 4 states that had no malpractice payments of at least $1 million reported to the NPDB: Alaska, Kansas, North Dakota, and Nebraska, with Kansas having the largest population. In states with at least one $1 million-plus malpractice payment, Texas physicians had the lowest rate per million population, 0.22—just 6 awards from a population of 27 million.

Reference
1. NPDB Research Statistics. National Practitioner Data Bank. http://www.npdb.hrsa.gov/resources/npdbstats/npdbStatistics.jsp. Accessed
July 17, 2015.

Copyright © 2015 Ob.Gyn. News Digital Network, Frontline Medical Communications. Available at: http://www.obgynews.com/?id=11146&tx_ttnews[tt_news]=417377&cHash=5cc8cd69fa7c8a1186aaeec0e814e4e4


The Obstetrics Closed Claims Study findings were released earlier this spring by the Napa, California−based Doctors Company, the nation’s largest physician-owned medical malpractice insurer.1 Susan Mann, MD,a spokesperson for the company, provided expert commentary on the study at the 2015 Annual Clinical Meeting of the American College of Obstetricians and Gynecologists in San Francisco (see “Frequent sources of malpractice claims” below).

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

Frequent sources of malpractice claims
Communication breakdowns and treatment delays are frequent sources of malpractice claims. Susan Mann, MD, spokesperson for The Doctors Company, the nation’s largest physician-owned medical malpractice insurer, discusses the underlying practice vulnerabilities revealed by the Obstetrics Closed Claims Study.
Dr. Mann practices obstetrics and gynecology in Brookline, Massachusetts, and at Beth Israel Deaconess Medical Center in Boston. She is president of the QualBridge Institute, a consulting firm focused on issues of quality and safety.


Top 7 factors contributing to patient injury
The Doctors Company identified specific factors that contributed to patient injury in the closed claims1:  

  1. Selection and management of therapy(34%). Among the issues here were decisions involving augmentation of labor, route of delivery, and the timing of interventions. This factor also related to medications—for example, a failure to order antibiotics for Group A and Group B strep, a failure to order Rho(D) immune globulin for Rh-negative mothers, and a failure to provide magnesium sulfate for women with eclampsia.
  2. Patient-assessment issues (32%). The Doctors Company reviewers found that physicians frequently failed to consider information that was available, or overlooked abnormal findings.
  3. Technical performance (18%). This factor involved problems associated with known risks of various procedures, such as postpartum hemorrhage and brachial plexus injuries. It also included poor technique.
  4. Communication problems among providers (17%).
  5. Patient factors (16%). These factors included a failure to comply with therapy or to show up for appointments.
  6. Insufficient notes or a lack of documentation (14%).
  7. Communication problems between patient/family and provider (14%).

“Studying obstetrical medical malpractice claims sheds light on the wide array of problems that may arise during pregnancy and in labor and delivery,” the study authors conclude. “Many of these cases reflect unusual maternal or neonatal conditions that can be diagnosed only with vigilance. Examples include protein deficiencies, clotting abnormalities, placental abruptions, infections, and genetic abnormalities. More common conditions should be identified with close attention to vital signs, laboratory studies, changes to maternal and neonatal conditions, and patient complaints.”1 See “Tips for reducing malpractice claims in obstetrics” below.

 

 

Tips for reducing malpractice claims in obstetrics1

The Obstetrics Closed Claim Study identified a number of “underlying vulnerabilities” that place patients at risk and increase liability for clinicians. The Doctors Company offers the following tips to help reduce these claims:

Require periodic training and certification for physicians and nurses to maintain competency and facilitate conversations about fetal heart-rate (FHR) tracing interpretation. Both parties should use the same terminology when discussing the strips.

Use technology that allows physicians to review FHR patterns from remote locations so that physicians and nurses are able to see the same information when discussing next steps.

When operative vaginal delivery is attempted in the face of a Category III FHR tracing, a contingency team should be available for possible emergent cesarean delivery.

Foster a culture in which caregivers feel comfortable speaking up if they have a concern. Ensure that the organization has a well-defined escalation guideline.


“Obstetric departments must plan for clinical emergencies by developing and maintaining physician and staff competencies through mock drills and simulations that reduce the likelihood of injuries to mothers and their infants,” the study authors conclude.1

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

References

Reference
1. The Doctors Company. Obstetrics Closed Claim Study. http://www.thedoctors.com/KnowledgeCenter/Pa tient Safety/articles/CON_ID_011803. Published April 2015. Accessed May 6, 2015. 

References

Reference
1. The Doctors Company. Obstetrics Closed Claim Study. http://www.thedoctors.com/KnowledgeCenter/Pa tient Safety/articles/CON_ID_011803. Published April 2015. Accessed May 6, 2015. 

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Janelle Yates, Susan Mann MD, American College of Obstetricians and Gynecologists, ACOG, QualBridge Institute, Doctors Company, medical malpractice, communication breakdowns, treatment delays, obstetric malpractice claims, fetal distress, improper performance of vaginal delivery, improper management of pregnancy, fetal heart-rate tracings, brachial plexus injury, shoulder dystocia, forceps delivery, vacuum extraction delivery, fetal abnormalities, complications of pregnancy, diagnosis-related claims, delay in delivery, improper performance of operative delivery, retained foreign bodies, improper choice of delivery method,insufficient documentation, patient-assessment issues, FHR, operative vaginal delivery, liability
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Janelle Yates, Susan Mann MD, American College of Obstetricians and Gynecologists, ACOG, QualBridge Institute, Doctors Company, medical malpractice, communication breakdowns, treatment delays, obstetric malpractice claims, fetal distress, improper performance of vaginal delivery, improper management of pregnancy, fetal heart-rate tracings, brachial plexus injury, shoulder dystocia, forceps delivery, vacuum extraction delivery, fetal abnormalities, complications of pregnancy, diagnosis-related claims, delay in delivery, improper performance of operative delivery, retained foreign bodies, improper choice of delivery method,insufficient documentation, patient-assessment issues, FHR, operative vaginal delivery, liability
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    In this Article

  • Tips for reducing malpractice claims in obstetrics
  • Where are the really big malpractice awards?
  • Top 7 factors contributing topatient injury
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July 2015 Quiz 2

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Critique

Patients with mild pancreatitis can be treated with hydration alone. Initial feeding with a low-fat diet is safe and may reduce the duration of hospitalization, compared with a clear liquid diet in patients with mild pancreatitis. Multiple studies have demonstrated that enteral feeding is safe and tolerated in acute pancreatitis. Additionally, enteral feeding may preserve gut barrier function and prevent translocation of bacteria, which are implicated in pancreatic infections. A meta-analysis of the existing literature has demonstrated improved outcome with enteral feeding, compared with parenteral feeding, with less infectious complications, reduced cost, and better glycemic control.

References

1. McClave, S.A., Change, W.K., Dhaliwal, R., et al. Nutritional support in acute pancreatitis; a systemic review of the literature. J. Parenteral Enteral Nutr. 2006;30:143–56.

2. Vu M.K., van der Veek P.P., Frolich M., et al. Does jejunal feeding activate exocrine pancreatic secretions? Eur. J. Clin. Invest. 1999;29:1053–9.

3. Petrov M.S., van Santvoort H.C., Besselink M.S., et al. Enteral nutrition and the risk of mortality and infectious complications in patients with severe acute pancreatitis: a meta-analysis of randomized trials. Arch. Surg. 2008;143:1111–7.

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Critique

Patients with mild pancreatitis can be treated with hydration alone. Initial feeding with a low-fat diet is safe and may reduce the duration of hospitalization, compared with a clear liquid diet in patients with mild pancreatitis. Multiple studies have demonstrated that enteral feeding is safe and tolerated in acute pancreatitis. Additionally, enteral feeding may preserve gut barrier function and prevent translocation of bacteria, which are implicated in pancreatic infections. A meta-analysis of the existing literature has demonstrated improved outcome with enteral feeding, compared with parenteral feeding, with less infectious complications, reduced cost, and better glycemic control.

References

1. McClave, S.A., Change, W.K., Dhaliwal, R., et al. Nutritional support in acute pancreatitis; a systemic review of the literature. J. Parenteral Enteral Nutr. 2006;30:143–56.

2. Vu M.K., van der Veek P.P., Frolich M., et al. Does jejunal feeding activate exocrine pancreatic secretions? Eur. J. Clin. Invest. 1999;29:1053–9.

3. Petrov M.S., van Santvoort H.C., Besselink M.S., et al. Enteral nutrition and the risk of mortality and infectious complications in patients with severe acute pancreatitis: a meta-analysis of randomized trials. Arch. Surg. 2008;143:1111–7.

Critique

Patients with mild pancreatitis can be treated with hydration alone. Initial feeding with a low-fat diet is safe and may reduce the duration of hospitalization, compared with a clear liquid diet in patients with mild pancreatitis. Multiple studies have demonstrated that enteral feeding is safe and tolerated in acute pancreatitis. Additionally, enteral feeding may preserve gut barrier function and prevent translocation of bacteria, which are implicated in pancreatic infections. A meta-analysis of the existing literature has demonstrated improved outcome with enteral feeding, compared with parenteral feeding, with less infectious complications, reduced cost, and better glycemic control.

References

1. McClave, S.A., Change, W.K., Dhaliwal, R., et al. Nutritional support in acute pancreatitis; a systemic review of the literature. J. Parenteral Enteral Nutr. 2006;30:143–56.

2. Vu M.K., van der Veek P.P., Frolich M., et al. Does jejunal feeding activate exocrine pancreatic secretions? Eur. J. Clin. Invest. 1999;29:1053–9.

3. Petrov M.S., van Santvoort H.C., Besselink M.S., et al. Enteral nutrition and the risk of mortality and infectious complications in patients with severe acute pancreatitis: a meta-analysis of randomized trials. Arch. Surg. 2008;143:1111–7.

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References

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A 65-year-old man is admitted with severe abdominal pain, fever, nausea, and vomiting. On examination, he is febrile, with stable vital signs. The upper abdomen is diffusely tender, with rebound and absent bowel sounds. Left flank ecchymosis is present. Serum amylase and lipase are elevated. After aggressive fluid resuscitation, a contrast CT scan on day 2 of illness demonstrates an edematous pancreas with nonenhancement of about 30% of the gland and multiple peripancreatic fluid collections. In terms of management, which of the following statements about nutrition is correct?
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Q1: ANSWER: B

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This patient has developed an ulcer because of chronic NSAID use. She is older than 60 years old and is also on antiplatelet therapy. Therefore, her risk of peptic ulcer rebleeding is high and warrants lifelong secondary prophylaxis with a proton pump inhibitor (Choice B). Therefore, stopping all prophylactic measures would be inappropriate (Choice A). Repeat endoscopy to assess for gastric ulcer healing may be warranted, especially in the setting of risk factors for malignancy, but duodenal ulcers do not require endoscopic follow-up (Choice C). There is no role to empirically treat H. pylori in the context of having negative test results (Choice E).

References

1. Bhatt, D.L., et al. ACCF/ACG/AHA 2008 Expert Consensus Document on Reducing the Gastrointestinal Risks of Antiplatelet Therapy and NSAID Use. Am. J. Gastroenterol. 2008;103:2890-907.


2. Abraham, N., et al. ACCF/ACG/AHA 2010 Expert Consensus Document on the Concomitant Use of Proton Pump Inhibitors and Thienopyridines: A Focused Update of the ACCF/ACG/AHA 2008 Expert Consensus Document on Reducing the Gastrointestinal Risks of Antiplatelet Therapy and NSAID Use. J. Am. Coll. Cardiol. 2010;56:2051-66.

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Q1: ANSWER: B

Critique

This patient has developed an ulcer because of chronic NSAID use. She is older than 60 years old and is also on antiplatelet therapy. Therefore, her risk of peptic ulcer rebleeding is high and warrants lifelong secondary prophylaxis with a proton pump inhibitor (Choice B). Therefore, stopping all prophylactic measures would be inappropriate (Choice A). Repeat endoscopy to assess for gastric ulcer healing may be warranted, especially in the setting of risk factors for malignancy, but duodenal ulcers do not require endoscopic follow-up (Choice C). There is no role to empirically treat H. pylori in the context of having negative test results (Choice E).

References

1. Bhatt, D.L., et al. ACCF/ACG/AHA 2008 Expert Consensus Document on Reducing the Gastrointestinal Risks of Antiplatelet Therapy and NSAID Use. Am. J. Gastroenterol. 2008;103:2890-907.


2. Abraham, N., et al. ACCF/ACG/AHA 2010 Expert Consensus Document on the Concomitant Use of Proton Pump Inhibitors and Thienopyridines: A Focused Update of the ACCF/ACG/AHA 2008 Expert Consensus Document on Reducing the Gastrointestinal Risks of Antiplatelet Therapy and NSAID Use. J. Am. Coll. Cardiol. 2010;56:2051-66.

Q1: ANSWER: B

Critique

This patient has developed an ulcer because of chronic NSAID use. She is older than 60 years old and is also on antiplatelet therapy. Therefore, her risk of peptic ulcer rebleeding is high and warrants lifelong secondary prophylaxis with a proton pump inhibitor (Choice B). Therefore, stopping all prophylactic measures would be inappropriate (Choice A). Repeat endoscopy to assess for gastric ulcer healing may be warranted, especially in the setting of risk factors for malignancy, but duodenal ulcers do not require endoscopic follow-up (Choice C). There is no role to empirically treat H. pylori in the context of having negative test results (Choice E).

References

1. Bhatt, D.L., et al. ACCF/ACG/AHA 2008 Expert Consensus Document on Reducing the Gastrointestinal Risks of Antiplatelet Therapy and NSAID Use. Am. J. Gastroenterol. 2008;103:2890-907.


2. Abraham, N., et al. ACCF/ACG/AHA 2010 Expert Consensus Document on the Concomitant Use of Proton Pump Inhibitors and Thienopyridines: A Focused Update of the ACCF/ACG/AHA 2008 Expert Consensus Document on Reducing the Gastrointestinal Risks of Antiplatelet Therapy and NSAID Use. J. Am. Coll. Cardiol. 2010;56:2051-66.

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An 80-year-old woman presents with melena after taking ibuprofen for osteoarthritis. She had an endoscopy that revealed a duodenal bulb ulcer. Biopsies for H. pylori were unremarkable, and the patient had serologic testing for H. pylori antibody, which was also negative. She has a prior history of a stroke and is on clopidogrel indefinitely. She was placed on pantoprazole 40 mg twice daily for 12 weeks. She returns to your office after 12 weeks and is feeling well.
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PHM15: How to Make Difficult Conversations Manageable

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Summary:

One of PHM15's first sessions was a workshop led by Dr. Rachna May focusing on the role of pediatric hospitalists in end-of-life conversations.

Medically complex pediatric patients are more likely to have end-of-life care in the hospital, placing the pediatric hospitalist in a unique position to address end-of-life issues. Medically complex patients may have waxing and waning courses, with frequent admissions for acute illness. Following these admissions, they may not fully return to their pre-illness baseline, leading to an overall gradual decline in health. An opportunity for discussing quality of life is available with each acute illness and hospitalization.

These conversations, however, can be difficult to initiate and present several barriers to overcome. These barriers include:

  • Unknown parental expectations regarding outcome,

  • Lack of an established relationship with the patient and family, and

  • Lack of readiness of the patient and family to discuss end-of-life decisions.

To overcome these barriers, providers must develop tools for delivery. They must find the right setting for the conversation, limit distractions, and avoid medical jargon. Begin with asking the patient and family's perceptions of the clinical prognosis and be honest when discussing the predicted medical outcomes for the patient. Open discussion of the prognosis allows autonomy in decision making, helps families feel supported, and can help them manage distress surrounding end-of-life care.

Such terminology as "do not resuscitate" can be interpreted as “doing nothing,” and result in feelings of guilt for a family desiring care for their child. Using a phrase such as "allowing a natural death" can alleviate feelings of guilt over end-of-life decisions and help the family actively provide care while optimizing quality of life. TH

Dr. Player is a hospitalist and assistant professor in the Department of Pediatrics at Medical College of Wisconsin, Children’s Hospital of Wisconsin in Milwaukee.

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Brittany Player, DO, MS
Author(s)
Brittany Player, DO, MS

Summary:

One of PHM15's first sessions was a workshop led by Dr. Rachna May focusing on the role of pediatric hospitalists in end-of-life conversations.

Medically complex pediatric patients are more likely to have end-of-life care in the hospital, placing the pediatric hospitalist in a unique position to address end-of-life issues. Medically complex patients may have waxing and waning courses, with frequent admissions for acute illness. Following these admissions, they may not fully return to their pre-illness baseline, leading to an overall gradual decline in health. An opportunity for discussing quality of life is available with each acute illness and hospitalization.

These conversations, however, can be difficult to initiate and present several barriers to overcome. These barriers include:

  • Unknown parental expectations regarding outcome,

  • Lack of an established relationship with the patient and family, and

  • Lack of readiness of the patient and family to discuss end-of-life decisions.

To overcome these barriers, providers must develop tools for delivery. They must find the right setting for the conversation, limit distractions, and avoid medical jargon. Begin with asking the patient and family's perceptions of the clinical prognosis and be honest when discussing the predicted medical outcomes for the patient. Open discussion of the prognosis allows autonomy in decision making, helps families feel supported, and can help them manage distress surrounding end-of-life care.

Such terminology as "do not resuscitate" can be interpreted as “doing nothing,” and result in feelings of guilt for a family desiring care for their child. Using a phrase such as "allowing a natural death" can alleviate feelings of guilt over end-of-life decisions and help the family actively provide care while optimizing quality of life. TH

Dr. Player is a hospitalist and assistant professor in the Department of Pediatrics at Medical College of Wisconsin, Children’s Hospital of Wisconsin in Milwaukee.

Summary:

One of PHM15's first sessions was a workshop led by Dr. Rachna May focusing on the role of pediatric hospitalists in end-of-life conversations.

Medically complex pediatric patients are more likely to have end-of-life care in the hospital, placing the pediatric hospitalist in a unique position to address end-of-life issues. Medically complex patients may have waxing and waning courses, with frequent admissions for acute illness. Following these admissions, they may not fully return to their pre-illness baseline, leading to an overall gradual decline in health. An opportunity for discussing quality of life is available with each acute illness and hospitalization.

These conversations, however, can be difficult to initiate and present several barriers to overcome. These barriers include:

  • Unknown parental expectations regarding outcome,

  • Lack of an established relationship with the patient and family, and

  • Lack of readiness of the patient and family to discuss end-of-life decisions.

To overcome these barriers, providers must develop tools for delivery. They must find the right setting for the conversation, limit distractions, and avoid medical jargon. Begin with asking the patient and family's perceptions of the clinical prognosis and be honest when discussing the predicted medical outcomes for the patient. Open discussion of the prognosis allows autonomy in decision making, helps families feel supported, and can help them manage distress surrounding end-of-life care.

Such terminology as "do not resuscitate" can be interpreted as “doing nothing,” and result in feelings of guilt for a family desiring care for their child. Using a phrase such as "allowing a natural death" can alleviate feelings of guilt over end-of-life decisions and help the family actively provide care while optimizing quality of life. TH

Dr. Player is a hospitalist and assistant professor in the Department of Pediatrics at Medical College of Wisconsin, Children’s Hospital of Wisconsin in Milwaukee.

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PHM15: Inter-Professional Approach to Patient Safety Training

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Akshata Hopkins, MD

Summary:

In an era where a majority of the pediatric hospital workforce is just starting to recognize fish bone diagrams, five why questions, root cause analysis, IHI, Lean, six sigma and pareto charts, hospitalists can be daunted as they try to serve as the home for quality improvement and patient safety in hospitals. Hospitalists are expected to know, understand, and practice these models for improvement with limited training and expertise. Beyond being looked at as experts, they are expected to teach residents and other learners when they are unsure of it ourselves. Governing education bodies (i.e., ACGME and CLER) have made it a requirement that residents have these concepts integrated into their curriculums and tracked.

Presented by an inter-professional team from Floating Hospital for Children at Tufts Medical Center in Boston, this PHM15 workshop focused on how to work in multidisciplinary teams to identify, analyze, and create patient-safety solutions, and, therefore, set the stage for systems- or department-based QI projects.

“It is OK to make mistakes, but it is not OK to not learn from them,” stated the presenters.

Starting with a near-miss event that led to a department/resident-led root cause analysis, the importance of system improvement became apparent. Presenters discussed the 12-week curriculum they created for pediatric residents and nursing students, which includes:

  • Didactics,

  • Online, self-directed learning, and

  • An inter-professional, small-group project.

Trainees present their analysis and action items to their departments and, at times, even administration. This helps align hospital goals with resident teaching, while simultaneously providing an environment where discussing errors safely in order to prevent further harms.

Attendees of the workshop walked away with a generalizable, step-by-step toolkit to take home to their home institution.

Key Takeaways:

  1. Convene a leadership team of nurses and physicians to develop the inter-professional program

  2. Consider scheduling demands of nurses, physicians and residents.

  3. Implement administrative support to assist with scheduling of meetings, maintenance of documents and email distribution.

  4. Program participation must bring value to the staff such as CME credits

  5. Make the educational experience program flexible in a blended learning environment.

  6. Recognize staff’s completion of the program with a certificate.

  7. Provide the opportunity, mentorship and support for staff willing to continue the project as a quality improvement initiative. TH

Dr. Hopkins is a pediatric hospitalist at All Children's Hospital Johns Hopkins Medicine, and an instructor at Johns Hopkins Medicine in St. Petersburg, Fla.

 

 

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Akshata Hopkins, MD
Author(s)
Akshata Hopkins, MD

Summary:

In an era where a majority of the pediatric hospital workforce is just starting to recognize fish bone diagrams, five why questions, root cause analysis, IHI, Lean, six sigma and pareto charts, hospitalists can be daunted as they try to serve as the home for quality improvement and patient safety in hospitals. Hospitalists are expected to know, understand, and practice these models for improvement with limited training and expertise. Beyond being looked at as experts, they are expected to teach residents and other learners when they are unsure of it ourselves. Governing education bodies (i.e., ACGME and CLER) have made it a requirement that residents have these concepts integrated into their curriculums and tracked.

Presented by an inter-professional team from Floating Hospital for Children at Tufts Medical Center in Boston, this PHM15 workshop focused on how to work in multidisciplinary teams to identify, analyze, and create patient-safety solutions, and, therefore, set the stage for systems- or department-based QI projects.

“It is OK to make mistakes, but it is not OK to not learn from them,” stated the presenters.

Starting with a near-miss event that led to a department/resident-led root cause analysis, the importance of system improvement became apparent. Presenters discussed the 12-week curriculum they created for pediatric residents and nursing students, which includes:

  • Didactics,

  • Online, self-directed learning, and

  • An inter-professional, small-group project.

Trainees present their analysis and action items to their departments and, at times, even administration. This helps align hospital goals with resident teaching, while simultaneously providing an environment where discussing errors safely in order to prevent further harms.

Attendees of the workshop walked away with a generalizable, step-by-step toolkit to take home to their home institution.

Key Takeaways:

  1. Convene a leadership team of nurses and physicians to develop the inter-professional program

  2. Consider scheduling demands of nurses, physicians and residents.

  3. Implement administrative support to assist with scheduling of meetings, maintenance of documents and email distribution.

  4. Program participation must bring value to the staff such as CME credits

  5. Make the educational experience program flexible in a blended learning environment.

  6. Recognize staff’s completion of the program with a certificate.

  7. Provide the opportunity, mentorship and support for staff willing to continue the project as a quality improvement initiative. TH

Dr. Hopkins is a pediatric hospitalist at All Children's Hospital Johns Hopkins Medicine, and an instructor at Johns Hopkins Medicine in St. Petersburg, Fla.

 

 

Summary:

In an era where a majority of the pediatric hospital workforce is just starting to recognize fish bone diagrams, five why questions, root cause analysis, IHI, Lean, six sigma and pareto charts, hospitalists can be daunted as they try to serve as the home for quality improvement and patient safety in hospitals. Hospitalists are expected to know, understand, and practice these models for improvement with limited training and expertise. Beyond being looked at as experts, they are expected to teach residents and other learners when they are unsure of it ourselves. Governing education bodies (i.e., ACGME and CLER) have made it a requirement that residents have these concepts integrated into their curriculums and tracked.

Presented by an inter-professional team from Floating Hospital for Children at Tufts Medical Center in Boston, this PHM15 workshop focused on how to work in multidisciplinary teams to identify, analyze, and create patient-safety solutions, and, therefore, set the stage for systems- or department-based QI projects.

“It is OK to make mistakes, but it is not OK to not learn from them,” stated the presenters.

Starting with a near-miss event that led to a department/resident-led root cause analysis, the importance of system improvement became apparent. Presenters discussed the 12-week curriculum they created for pediatric residents and nursing students, which includes:

  • Didactics,

  • Online, self-directed learning, and

  • An inter-professional, small-group project.

Trainees present their analysis and action items to their departments and, at times, even administration. This helps align hospital goals with resident teaching, while simultaneously providing an environment where discussing errors safely in order to prevent further harms.

Attendees of the workshop walked away with a generalizable, step-by-step toolkit to take home to their home institution.

Key Takeaways:

  1. Convene a leadership team of nurses and physicians to develop the inter-professional program

  2. Consider scheduling demands of nurses, physicians and residents.

  3. Implement administrative support to assist with scheduling of meetings, maintenance of documents and email distribution.

  4. Program participation must bring value to the staff such as CME credits

  5. Make the educational experience program flexible in a blended learning environment.

  6. Recognize staff’s completion of the program with a certificate.

  7. Provide the opportunity, mentorship and support for staff willing to continue the project as a quality improvement initiative. TH

Dr. Hopkins is a pediatric hospitalist at All Children's Hospital Johns Hopkins Medicine, and an instructor at Johns Hopkins Medicine in St. Petersburg, Fla.

 

 

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PHM15: Effective Intranasal Sedation

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Travis W. Crook, MD

Presenters: Kelly Basaldua, MD; Daniel Sedillo, MD, MBA, and Jason Reynolds, MD

Summary:

In an environment where medicine is becoming ever more specialized and the scope of practice for many is ever narrowing into corridors of expertise, the hospitalist remains a bastion of generalism with an ever-diversifying skill set. One of the skills acquired by many hospitalists to aid in the overall efficiency of the hospital is intranasal (IN) sedation.

Intranasal sedation is becoming more popular given the rapid onset and offset and the relative safety of the sedation of patients without the need for intravenous catheters. This phenomenon is accomplished by avoiding the gut and thus avoiding first-pass metabolism. This allows for greatly increased bioavailability compared with oral administration. In addition, the nasal mucosa is in near direct contact with the CSF via the cribriform plate, allowing for rapid and effective action.

To maximize the effectiveness of intranasal sedation, low volumes with high concentrations, atomization, and minimal nasal occlusion are vital. The ideal volume per nostril is approximately 0.5 ml as using any greater volume results in oversaturation and minimal additional absorption. Thus, concentrating the medications into minimal volumes provides for more efficacious usage. Atomization aids in ensuring thorough surface area coverage and higher absorption. This is a far more efficacious method of delivery than liquid/drop administration.

Because intranasally administered agents have a delayed and widened serum peak compared to IV, IN sedation carries less of a chance to reach serum levels high enough to cause respiratory depression, though monitoring is still necessary. When compared to IV sedation, IN does have a delay in onset, but also provides for a more gentle recovery process, often resulting in a less disorienting recovery for the patient, while also providing for a wider safety profile.

The presenters covered three primary agents:

  • midazolam,

  • dexmedetomidine, and

  • fentanyl

Midazolam is useful for non-painful, minimally invasive procedures. Fentanyl is more useful for painful or more invasive procedures. Dexmedetomidine is off-label use for intranasal sedation at this time, but has promising initial research given its safety profile and longer duration of action compared to most intranasal agents. Also, dexmedetomidine works extremely effectively in combination with other agents, particularly midazolam, to prolong sedations, making it very useful for longer procedures like combination MRIs.

The presenters then provided a practical workshop to practice the delivery of intranasal medication effectively. One of the pearls provided involved proper positioning of the patient in a reclined position as sitting to erect will cause the medication to drip out and having the patient lying flat will result in the medication dripping down the posterior pharynx. This position should be held for 30 seconds after delivery of the medication. Practicing with atomizers to achieve effective aerosolization was discussed. The target of medication should avoid the nasal septum given its poor absorption.

Key Takeaway:

With hospitalists being called to assist in ever-expanding roles within the hospital system while improving efficiency and throughput, intranasal sedation may provide reduced imaging wait times, bedside and ED procedure times in a safe and effective manner. TH

Dr. Crook is a hospitalist in the division of hospitalist medicine, assistant professor of pediatrics, and assistant pediatric clerkship director in the Department of Pediatrics at Vanderbilt University School of Medicine and Monroe Carell Jr. Children's Hospital at Vanderbilt in Nashville.

 

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Travis W. Crook, MD
Author(s)
Travis W. Crook, MD

Presenters: Kelly Basaldua, MD; Daniel Sedillo, MD, MBA, and Jason Reynolds, MD

Summary:

In an environment where medicine is becoming ever more specialized and the scope of practice for many is ever narrowing into corridors of expertise, the hospitalist remains a bastion of generalism with an ever-diversifying skill set. One of the skills acquired by many hospitalists to aid in the overall efficiency of the hospital is intranasal (IN) sedation.

Intranasal sedation is becoming more popular given the rapid onset and offset and the relative safety of the sedation of patients without the need for intravenous catheters. This phenomenon is accomplished by avoiding the gut and thus avoiding first-pass metabolism. This allows for greatly increased bioavailability compared with oral administration. In addition, the nasal mucosa is in near direct contact with the CSF via the cribriform plate, allowing for rapid and effective action.

To maximize the effectiveness of intranasal sedation, low volumes with high concentrations, atomization, and minimal nasal occlusion are vital. The ideal volume per nostril is approximately 0.5 ml as using any greater volume results in oversaturation and minimal additional absorption. Thus, concentrating the medications into minimal volumes provides for more efficacious usage. Atomization aids in ensuring thorough surface area coverage and higher absorption. This is a far more efficacious method of delivery than liquid/drop administration.

Because intranasally administered agents have a delayed and widened serum peak compared to IV, IN sedation carries less of a chance to reach serum levels high enough to cause respiratory depression, though monitoring is still necessary. When compared to IV sedation, IN does have a delay in onset, but also provides for a more gentle recovery process, often resulting in a less disorienting recovery for the patient, while also providing for a wider safety profile.

The presenters covered three primary agents:

  • midazolam,

  • dexmedetomidine, and

  • fentanyl

Midazolam is useful for non-painful, minimally invasive procedures. Fentanyl is more useful for painful or more invasive procedures. Dexmedetomidine is off-label use for intranasal sedation at this time, but has promising initial research given its safety profile and longer duration of action compared to most intranasal agents. Also, dexmedetomidine works extremely effectively in combination with other agents, particularly midazolam, to prolong sedations, making it very useful for longer procedures like combination MRIs.

The presenters then provided a practical workshop to practice the delivery of intranasal medication effectively. One of the pearls provided involved proper positioning of the patient in a reclined position as sitting to erect will cause the medication to drip out and having the patient lying flat will result in the medication dripping down the posterior pharynx. This position should be held for 30 seconds after delivery of the medication. Practicing with atomizers to achieve effective aerosolization was discussed. The target of medication should avoid the nasal septum given its poor absorption.

Key Takeaway:

With hospitalists being called to assist in ever-expanding roles within the hospital system while improving efficiency and throughput, intranasal sedation may provide reduced imaging wait times, bedside and ED procedure times in a safe and effective manner. TH

Dr. Crook is a hospitalist in the division of hospitalist medicine, assistant professor of pediatrics, and assistant pediatric clerkship director in the Department of Pediatrics at Vanderbilt University School of Medicine and Monroe Carell Jr. Children's Hospital at Vanderbilt in Nashville.

 

Presenters: Kelly Basaldua, MD; Daniel Sedillo, MD, MBA, and Jason Reynolds, MD

Summary:

In an environment where medicine is becoming ever more specialized and the scope of practice for many is ever narrowing into corridors of expertise, the hospitalist remains a bastion of generalism with an ever-diversifying skill set. One of the skills acquired by many hospitalists to aid in the overall efficiency of the hospital is intranasal (IN) sedation.

Intranasal sedation is becoming more popular given the rapid onset and offset and the relative safety of the sedation of patients without the need for intravenous catheters. This phenomenon is accomplished by avoiding the gut and thus avoiding first-pass metabolism. This allows for greatly increased bioavailability compared with oral administration. In addition, the nasal mucosa is in near direct contact with the CSF via the cribriform plate, allowing for rapid and effective action.

To maximize the effectiveness of intranasal sedation, low volumes with high concentrations, atomization, and minimal nasal occlusion are vital. The ideal volume per nostril is approximately 0.5 ml as using any greater volume results in oversaturation and minimal additional absorption. Thus, concentrating the medications into minimal volumes provides for more efficacious usage. Atomization aids in ensuring thorough surface area coverage and higher absorption. This is a far more efficacious method of delivery than liquid/drop administration.

Because intranasally administered agents have a delayed and widened serum peak compared to IV, IN sedation carries less of a chance to reach serum levels high enough to cause respiratory depression, though monitoring is still necessary. When compared to IV sedation, IN does have a delay in onset, but also provides for a more gentle recovery process, often resulting in a less disorienting recovery for the patient, while also providing for a wider safety profile.

The presenters covered three primary agents:

  • midazolam,

  • dexmedetomidine, and

  • fentanyl

Midazolam is useful for non-painful, minimally invasive procedures. Fentanyl is more useful for painful or more invasive procedures. Dexmedetomidine is off-label use for intranasal sedation at this time, but has promising initial research given its safety profile and longer duration of action compared to most intranasal agents. Also, dexmedetomidine works extremely effectively in combination with other agents, particularly midazolam, to prolong sedations, making it very useful for longer procedures like combination MRIs.

The presenters then provided a practical workshop to practice the delivery of intranasal medication effectively. One of the pearls provided involved proper positioning of the patient in a reclined position as sitting to erect will cause the medication to drip out and having the patient lying flat will result in the medication dripping down the posterior pharynx. This position should be held for 30 seconds after delivery of the medication. Practicing with atomizers to achieve effective aerosolization was discussed. The target of medication should avoid the nasal septum given its poor absorption.

Key Takeaway:

With hospitalists being called to assist in ever-expanding roles within the hospital system while improving efficiency and throughput, intranasal sedation may provide reduced imaging wait times, bedside and ED procedure times in a safe and effective manner. TH

Dr. Crook is a hospitalist in the division of hospitalist medicine, assistant professor of pediatrics, and assistant pediatric clerkship director in the Department of Pediatrics at Vanderbilt University School of Medicine and Monroe Carell Jr. Children's Hospital at Vanderbilt in Nashville.

 

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PHM15: Preparing for Global Health Experiences

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David M. Pressel, MD, PhD

Presenters: Gitanjli Arora, Phuc Le, and Christiana Russ

Summary:

Overseas medical missions can be rewarding experiences for both trainees as part of a supervised program and attending physicians. There is substantial inequity in the global distribution of disease versus health care providers with most providers being located in developed countries and higher disease burdens in underdeveloped countries.  The goal of global healthcare training is mutual benefit, where the provider gains clinical experience and the host country gains enhanced medical care. Both provider and hosts gain increased cultural awareness.

The American Academy of Pediatrics guidelines for a meaningful international experience recommend 4 components:

  • Pre-trip Training.  Don’t go without some idea of what to expect

  • Pre-travel preparations.  Get your vaccines, travel plans, licensure, scope of practice taken care of.

  • Preceptorship by host and US faculty

  • Post-travel evaluation and feedback

Key Takeaways:

Providers in overseas medical missions will encounter challenging situations—culturally, ethically and medically. Get as much information beforehand. Be respectful of different cultural norms. Get a cultural ambassador. Keep in mind the Serenity Prayer. TH

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David M. Pressel, MD, PhD
Author(s)
David M. Pressel, MD, PhD

Presenters: Gitanjli Arora, Phuc Le, and Christiana Russ

Summary:

Overseas medical missions can be rewarding experiences for both trainees as part of a supervised program and attending physicians. There is substantial inequity in the global distribution of disease versus health care providers with most providers being located in developed countries and higher disease burdens in underdeveloped countries.  The goal of global healthcare training is mutual benefit, where the provider gains clinical experience and the host country gains enhanced medical care. Both provider and hosts gain increased cultural awareness.

The American Academy of Pediatrics guidelines for a meaningful international experience recommend 4 components:

  • Pre-trip Training.  Don’t go without some idea of what to expect

  • Pre-travel preparations.  Get your vaccines, travel plans, licensure, scope of practice taken care of.

  • Preceptorship by host and US faculty

  • Post-travel evaluation and feedback

Key Takeaways:

Providers in overseas medical missions will encounter challenging situations—culturally, ethically and medically. Get as much information beforehand. Be respectful of different cultural norms. Get a cultural ambassador. Keep in mind the Serenity Prayer. TH

Presenters: Gitanjli Arora, Phuc Le, and Christiana Russ

Summary:

Overseas medical missions can be rewarding experiences for both trainees as part of a supervised program and attending physicians. There is substantial inequity in the global distribution of disease versus health care providers with most providers being located in developed countries and higher disease burdens in underdeveloped countries.  The goal of global healthcare training is mutual benefit, where the provider gains clinical experience and the host country gains enhanced medical care. Both provider and hosts gain increased cultural awareness.

The American Academy of Pediatrics guidelines for a meaningful international experience recommend 4 components:

  • Pre-trip Training.  Don’t go without some idea of what to expect

  • Pre-travel preparations.  Get your vaccines, travel plans, licensure, scope of practice taken care of.

  • Preceptorship by host and US faculty

  • Post-travel evaluation and feedback

Key Takeaways:

Providers in overseas medical missions will encounter challenging situations—culturally, ethically and medically. Get as much information beforehand. Be respectful of different cultural norms. Get a cultural ambassador. Keep in mind the Serenity Prayer. TH

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PHM15: Management of Childhood Severe Acute Malnutrition

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Bethany Hodge, MD, MPH

Presenters: Sarah White MD, Mark Corden, MD, and Parminder Suchdev, MD, MPH

Summary:

This PHM15 workshop kicked off the Global Health pathway. The speakers explained that they had become interested in nutrition through the international experiences they had in the past with malnourished children around the world.

The learning objectives included reviewing:

  • Criteria for admission of malnourished children to feeding centers or inpatient care for severe acute malnutrition (SAM);

  • Micronutrient deficiencies in SAM;

  • Specific things to look for when treating SAM using rehydration and refeeding protocols;

  • Definitions and classification of malnutrition states; and

  • The burden disease malnutrition represents in global children’s health, as well as its association with increased mortality.

 

The presenters used case studies to give specific examples of how malnutrition complicates children’s health. Mid-upper arm circumference (MUAC) was reviewed as a proxy measure to quickly identify children at risk for malnutrition as well as the need for length and weight to fully describe the nutritional/growth state of a child. “Appetite test” was introduced as a way to assess if children have capability to try to increase feeding at home (if access to food is assured) or if they are experiencing a malnutrition state that would benefit from inpatient management. Comorbidities, such as edema, shock, and infections, were considered as reasons to admit the patient for malnutrition rated illness. WHO guidelines for use of specific refeeding formulas [PDF] and therapeutic ready-to-use food (RUTF) to manage stabilization versus transition phases were also reviewed.

 

In caring for acutely malnourished children, providers also need to be prepared to manage refeeding syndrome. It can be confused with sepsis due to both conditions presenting with acute decompensation of the patient, so it is important to keep in mind. Dehydrated malnourished children have very specialized needs, are sodium sensitive and are at risk of heart failure and pulmonary edema with typical rehydration methods. ReSoMal rehydration solution was described as an oral rehydration solution and lactated ringers IV for use in the management of a dehydrated, malnourished child.

 

Other topics covered in the workshop included the implications of the presence of edema in a malnourished patient, the use of antibiotics in improving mortality, and need for replenishing micronutrient stores. Overall, the workshop had an effective use of cases to show specific complications that a health care provider may encounter when treating children with SAM. TH

Dr. Hodge is a pediatric hospitalist at Kosair Children’s Hospital in Louisville, Ky., an assistant professor in the department of pediatrics, and director of distinction in global health track at the University of Louisville School of Medicine.

 

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Bethany Hodge, MD, MPH
Author(s)
Bethany Hodge, MD, MPH

Presenters: Sarah White MD, Mark Corden, MD, and Parminder Suchdev, MD, MPH

Summary:

This PHM15 workshop kicked off the Global Health pathway. The speakers explained that they had become interested in nutrition through the international experiences they had in the past with malnourished children around the world.

The learning objectives included reviewing:

  • Criteria for admission of malnourished children to feeding centers or inpatient care for severe acute malnutrition (SAM);

  • Micronutrient deficiencies in SAM;

  • Specific things to look for when treating SAM using rehydration and refeeding protocols;

  • Definitions and classification of malnutrition states; and

  • The burden disease malnutrition represents in global children’s health, as well as its association with increased mortality.

 

The presenters used case studies to give specific examples of how malnutrition complicates children’s health. Mid-upper arm circumference (MUAC) was reviewed as a proxy measure to quickly identify children at risk for malnutrition as well as the need for length and weight to fully describe the nutritional/growth state of a child. “Appetite test” was introduced as a way to assess if children have capability to try to increase feeding at home (if access to food is assured) or if they are experiencing a malnutrition state that would benefit from inpatient management. Comorbidities, such as edema, shock, and infections, were considered as reasons to admit the patient for malnutrition rated illness. WHO guidelines for use of specific refeeding formulas [PDF] and therapeutic ready-to-use food (RUTF) to manage stabilization versus transition phases were also reviewed.

 

In caring for acutely malnourished children, providers also need to be prepared to manage refeeding syndrome. It can be confused with sepsis due to both conditions presenting with acute decompensation of the patient, so it is important to keep in mind. Dehydrated malnourished children have very specialized needs, are sodium sensitive and are at risk of heart failure and pulmonary edema with typical rehydration methods. ReSoMal rehydration solution was described as an oral rehydration solution and lactated ringers IV for use in the management of a dehydrated, malnourished child.

 

Other topics covered in the workshop included the implications of the presence of edema in a malnourished patient, the use of antibiotics in improving mortality, and need for replenishing micronutrient stores. Overall, the workshop had an effective use of cases to show specific complications that a health care provider may encounter when treating children with SAM. TH

Dr. Hodge is a pediatric hospitalist at Kosair Children’s Hospital in Louisville, Ky., an assistant professor in the department of pediatrics, and director of distinction in global health track at the University of Louisville School of Medicine.

 

Presenters: Sarah White MD, Mark Corden, MD, and Parminder Suchdev, MD, MPH

Summary:

This PHM15 workshop kicked off the Global Health pathway. The speakers explained that they had become interested in nutrition through the international experiences they had in the past with malnourished children around the world.

The learning objectives included reviewing:

  • Criteria for admission of malnourished children to feeding centers or inpatient care for severe acute malnutrition (SAM);

  • Micronutrient deficiencies in SAM;

  • Specific things to look for when treating SAM using rehydration and refeeding protocols;

  • Definitions and classification of malnutrition states; and

  • The burden disease malnutrition represents in global children’s health, as well as its association with increased mortality.

 

The presenters used case studies to give specific examples of how malnutrition complicates children’s health. Mid-upper arm circumference (MUAC) was reviewed as a proxy measure to quickly identify children at risk for malnutrition as well as the need for length and weight to fully describe the nutritional/growth state of a child. “Appetite test” was introduced as a way to assess if children have capability to try to increase feeding at home (if access to food is assured) or if they are experiencing a malnutrition state that would benefit from inpatient management. Comorbidities, such as edema, shock, and infections, were considered as reasons to admit the patient for malnutrition rated illness. WHO guidelines for use of specific refeeding formulas [PDF] and therapeutic ready-to-use food (RUTF) to manage stabilization versus transition phases were also reviewed.

 

In caring for acutely malnourished children, providers also need to be prepared to manage refeeding syndrome. It can be confused with sepsis due to both conditions presenting with acute decompensation of the patient, so it is important to keep in mind. Dehydrated malnourished children have very specialized needs, are sodium sensitive and are at risk of heart failure and pulmonary edema with typical rehydration methods. ReSoMal rehydration solution was described as an oral rehydration solution and lactated ringers IV for use in the management of a dehydrated, malnourished child.

 

Other topics covered in the workshop included the implications of the presence of edema in a malnourished patient, the use of antibiotics in improving mortality, and need for replenishing micronutrient stores. Overall, the workshop had an effective use of cases to show specific complications that a health care provider may encounter when treating children with SAM. TH

Dr. Hodge is a pediatric hospitalist at Kosair Children’s Hospital in Louisville, Ky., an assistant professor in the department of pediatrics, and director of distinction in global health track at the University of Louisville School of Medicine.

 

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PHM15: Management of Childhood Severe Acute Malnutrition
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