To a very large extent the microbial agents responsible for infections or infectious complications after trauma are the same agents that cause most other surgical or ICU-associated infections. Table 18-1 shows the most common infectious agents that cause trauma-associated infections at various anatomic sites. Generally, Staphylococcus spp. and Streptococcus spp. are the most common pathogens responsible for infections in which the traumatic injury or operative intervention needed to treat the injury did not transgress a mucosal surface. For traumatic injuries that involve the aerodigestive tract the most common isolates are E. coli (43.4%), S. aureus (18.9%), Klebsiella pneumoniae (14.4%), and Enterococcus faecalis (5.6%).1 Hospitalized trauma patients develop nosocomial bacterial infections from the usual ICU-associated pathogens (Table 18-3). A few infectious agents that can be associated with trauma are seldom encountered in other settings including rabies virus, Clostridium tetani, and Vibrio spp. We will also discuss some of the unique challenges and concerns that have been brought to the attention of surgeons during the Ebola outbreak of 2014.
TABLE 18-3ICU Pathogens Isolated from Patients with Ventilator-Associated Pneumonia ||Download (.pdf) TABLE 18-3 ICU Pathogens Isolated from Patients with Ventilator-Associated Pneumonia
|Organism/Class ||% Total |
|Lactose-fermenting gram-negative bacillus |
| Escherichia coli ||8.1% |
| Klebsiella sp. ||11.1% |
| Enterobacter sp. ||7.6% |
| Morganella sp. ||0.5% |
| Citrobacter sp. ||1.0% |
| Serratia sp. ||1.5% |
|Lactose-non-fermenting gram-negative bacillus |
| Stenotrophomonas sp. || 2.0% |
| Acinetobacter sp. || 8.6% |
| Pseudomonas sp. ||13.6% |
| Staphylococcus aureus ||31.8% total |
| Methicillin-sensitive ||22.2% |
| Methicillin-resistant ||9.6% |
|Community pathogens |
| Streptococcus pneumonia ||2.0% |
| Haemophilus sp. ||3.0% |
|Other pathogens |
| Polymicrobial species ||3.0% |
| Fungus ||1.5% |
Rabies is a rare, potentially fatal, clinical disease caused by the rabies virus. Rabies is an RNA virus present in the saliva of mammals and transmission to humans generally occurs following a bite from a rabid animal. Prior to the development of a vaccine by Louis Pasteur, bites from a rabid animal were uniformly fatal. In North America, raccoons, skunks, bats, foxes, coyotes, and bobcats are the primary reservoirs. Most patients with rabies have no documented exposure to a rabid animal, and the majority of these are associated with bat bites. Many victims underestimate the importance of a bat bite and a substantial portion do not even recall being bitten. Bats (Carnivora and Chiroptera) represent the ultimate zoonotic reservoir for the virus, as well. The rabies virus is highly labile and can be inactivated readily by ultraviolet radiation, heat, desiccation, and other environmental factors.
The word “rabies” derives from the Latin rabere meaning “to rage” and refers to the clinical manifestations of the disease that include hyperactivity, disorientation, hallucinations, and bizarre behavior. The rabies virus is neurotropic and causes an acute encephalitis. Other hallmarks of the disease include an intense fear of suffocation (eg, hydrophobia and aerophobia) secondary to intense laryngeal and pharyngeal spasm. Once the patient begins manifesting symptoms death is nearly certain. With increased vaccination and postexposure prophylaxis (PEP) over the past 50 years, the clinical disease is becoming increasingly uncommon. According to the Centers for Disease Control and Prevention (CDC) 49 cases of human rabies were reported in the United States between 1995 and 2011, with only 3 survivors. That said, it is important for the practitioner of emergency medicine/surgery to be knowledgeable about rabies since animal bites are encountered frequently in clinical practice.
Humans are not routinely vaccinated against rabies, while domestic animals receive routine rabies vaccinations. If a human is bitten by a rabid animal, rabies can be prevented by PEP before the virus enters the central nervous system during the incubation period. The diagnosis of rabies can be made rapidly by identification of rabies virus in the brain of a potentially infected animal. This procedure can be performed most expeditiously by euthanizing the suspected animal. If the rabies test is negative, then no postexposure vaccination or prophylaxis is needed. The incidence of positive rabies tests ranges from as high as 6–10% in wild animals down to levels of ~1% in domestic pets. An acceptable alternative approach, if the suspected source is a domestic pet (dog, cat, ferret, etc.), is for the offending animal to be quarantined and observed for 10 days. If the animal exhibits signs of rabies, the exposed person should begin PEP immediately and the animal should be euthanized and its brain tissue tested for rabies. If the animal is confirmed to have rabies, PEP must be completed; however, if the test results are negative PEP can cease.
Immediate measures that should be taken to decrease the risk of rabies transmission include thorough washing of bite and scratch wounds with soap and water, followed by application of povidone–iodine or alcohol. Human rabies immune globulin (HRIG) and rabies vaccine should be given in all cases except in persons who have been immunized previously.18 Immune globulin should never be delivered in the same syringe as the vaccine, as this will cause precipitation. The Advisory Committee on Immunization Practices (ACIP) of the CDC and the American Academy of Pediatrics recommend a single dose (20 IU/kg) of HRIG be given to provide protection for the first 2 weeks until the vaccine elicits an antibody response. Detailed and up-to-date information for rabies exposure is available on the CDC’s Web site (http://www.cdc.gov/rabies/index.html), and this site should be consulted for the latest information. The ACIP recommends a regimen of human diploid cell vaccine (Imovax®) for PEP on days 0, 3, 7, 14, and 28 along with a single dose of HRIG on day 0. Once initiated, rabies prophylaxis should not be interrupted or discontinued because of local or mild systemic reactions to the vaccine.
Tetanus is a rare, life-threatening condition that is caused by toxins produced by Clostridium tetani, a spore-forming, gram-positive bacillus.19 Clostridial spores can survive indefinitely, and they are ubiquitous in soil and feces. Under anaerobic conditions the spores can germinate into mature bacilli that elaborate the neurotoxins tetanospasmin and tetanolysin. Tetanospasmin produces most prominent clinical symptoms by interfering with motor neuron release of the inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and glycine. The resulting loss of inhibition produces muscle spasm (usually spasm of the masseter muscle) and severe autonomic over-activity manifested by high fever, tachycardia, and hypertension. Historically, tetanus was highly fatal, but intensive medical therapy with neuromuscular blockade, mechanical ventilation, and ICU monitoring has lowered the case fatality rate to 11–28%. According to the CDC there were a total of 233 tetanus cases reported in the United States between 2001 and 2008, with 71.7% arising from acute trauma. Clinicians and trauma surgeons must remain alert for the potential of Clostridial contamination and provide appropriate, timely tetanus prophylaxis.19
The diagnosis of tetanus is made on clinical grounds alone, as there are no laboratory tests that can diagnose the condition or rule it out. Tetanus immunization is accomplished as a component of standard early childhood immunizations (diphtheria–pertussis–tetanus [DPT]), with administration of tetanus toxoid (TT) every 5–10 years to maintain immune memory (see, http://www.cdc.gov/tetanus/vaccination.html). No deaths have been reported in individuals who have been fully immunized. The CDC recommendations for tetanus prophylaxis depend on the wound characteristics and the prior immunization status of the patient. A wound with extensive contamination, one that is poorly vascularized, or with extensive soft tissue trauma is considered to be a “tetanus-prone wound.” A tetanus booster should be administered to patients who have received primary immunization, but who have not received TT during the past 10 years, or the past 5 years for tetanus-prone wounds.18 In patients who have never undergone primary immunization, human tetanus immune globulin (HTIG) should be administered along with TT at a different site. Antitetanus antibody binds to exotoxins and neutralizes their toxicity. High-risk groups such as the elderly, individuals with human immunodeficiency virus (HIV), and intravenous drug users (IVDU) who had received primary vaccination may not have tetanus antibodies, and more liberal use of HTIG should be considered in these groups.18
Infections Associated with Marine Trauma
Vibrio vulnificus is a gram-negative rod present in seawater that can result in atypical, necrotizing soft tissue infections when traumatic injuries occur in the ocean.20,21,22 V. vulnificus is common in warm seawater and thrives in water temperatures greater than 68°F (20°C). The organism is not associated with pollution or fecal waste. Approximately 25% of V. vulnificus infections are caused by direct exposure of an open wound to warm seawater containing the organism. Exposure typically occurs when the patient is participating in water activities such as boating, fishing, or swimming. Infections are occasionally attributed to contact with raw seafood or marine wildlife. The risk of developing Vibrio infection is much higher in immunocompromised patients or patients with preexisting hepatic disease or diabetes mellitus.21 Established infection with V. vulnificus can be highly invasive with mortality rates of 30–40% and a mortality greater than 50% in immunocompromised patients. A published report from 2009 documented a 37% mortality rate even after implementation of a specific treatment guideline for necrotizing Vibrio infections.20
Patients with wound infections caused by V. vulnificus develop painful cellulitis that progresses rapidly.21,22,23 Physical examination will often reveal marked swelling and painful, hemorrhagic bullae surrounding traumatic wounds. In some cases, there can be rapid progression and associated systemic symptoms. Marked local tissue swelling with hemorrhagic bullae is characteristic. Systemic symptoms include fever and chills, and bacteria are present in the bloodstream in more than 50% of patients. Hypotension or septic shock may be an early symptom, and alterations in mental status occur in approximately one-third of patients. Table 18-4 summarizes clinical symptoms present in patients with Vibrio infection. It is important for trauma surgeons to be aware of the potential for Vibrio infections in the appropriate clinical setting, because antibiotic treatment is distinctly different from the agents typically employed for trauma patients. Aggressive surgical debridement, incision and drainage of purulent collections, and even amputation may be crucial adjuncts for management of these often severe soft tissue infections.21 Recent experience in 30 patients with documented Vibrio infection found that fasciotomy was needed in all patients, and 17% required amputation.20 Recommended antibiotics include doxycycline (100 mg iv/po bid), ceftazidime (2 g q 8 hours), cefotaxime (2 g q 8 hours), or ciprofloxacin (750 mg po bid or 400 mg iv q 12 hours).21,24
TABLE 18-4Clinical Characteristics Associated with Vibrio vulnificus Wound Infections ||Download (.pdf) TABLE 18-4 Clinical Characteristics Associated with Vibrio vulnificus Wound Infections
|Characteristic ||% Patients |
|Cellulitis at wound site ||88 |
|Skin bullae ||88 |
|Fever (>37.8°C) ||65 |
|Chills ||29 |
|Ecchymosis ||18 |
|Obtundation, disorientation, or lethargy ||18 |
|Hypotension (<90 mm Hg) ||12 |
|Vomiting || 6 |
|Diarrhea || 6 |
Traumatic injuries that occur in freshwater conditions may develop infections from Aeromonas hydrophila.23 A. hydrophila is a gram-negative anaerobic rod that is a common pathogen of fish and amphibians. Cutaneous inoculation of the organism can result in cellulitis, abscesses and, occasionally, necrotizing soft tissue infections. Like the situation with Vibrio infections, patients with hepatic disease and immune-compromise have a greater risk of developing generalized disease. A. hydrophila can be recovered from the bloodstream in a significant proportion of patients and this fact, along with a history of injury in fresh water, will aid in alerting clinicians to the correct diagnosis. Antibiotic agents active against A. hydrophila include third-generation cephalosporins, fluoroquinolones, doxycycline, or trimethoprim–sulfamethoxazole.23
On September 30, 2014, in the midst of the worst ebola virus disease (EVD) outbreak on record,25 the Centers for Disease Control (CDC) confirmed the first documented case of EVD in the United States in Dallas, Texas. Within 2 weeks a nurse who cared for that initial patient was also diagnosed with the disease. While EVD is not a surgical disease per se, surgeons knowledge and skills in resuscitation, critical care, and disaster management may be invaluable in the treatment of EVD. Therefore all surgeons should be familiar with the fundamentals of EVD management.
Ebola virus is a zoonosis belonging to the Filoviridae family. Five species have been identified as follows: Zaire, Sudan, Ivory Coast, Bundibugyo, and Reston.26 Ebola is a single-stranded RNA virus that sporadically spreads to humans from a presumptive animal or bat reservoir in the wild. Human spread only occurs through direct contact with infected bodily fluid, and the most infectious sources are blood, feces, and vomit.27 Ebola virus can remain viable on surfaces for 1–6 days, although the risk of transmission from a surface contact is considered very low.28,29 Humans are only contagious while they are symptomatic. Blood from patients with untreated late EVD harbor 109 virus particles per mL, making it highly infectious. This value can be compared to the much lower viral loads in patients with untreated HIV (105/mL blood) or Hepatitis C (5–20 × 106/mL blood), both of which are recognized as being highly transmissible.30 EVD is not an airborne pathogen, but, since it can be transmitted via large droplets, health care providers in close contact with symptomatic patients should take necessary droplet precautions (See Prevention).31
Ebola virus enters the body through breaks in the skin, mucus membranes or ingestion and then infiltrates cells, especially lymph tissues, liver, and spleen. The virus continues to replicate until cells become necrotic and lyse, spilling more viral particles into the circulation. Ebola virus elicits a profound proinflammatory cytokine and chemokine response producing a vigorous SIRS reaction.32,33 Significant endothelial injury ensues, with loss of vascular tone and increased vascular permeability leading to hypotension and shock.34,35 At the end stages of disease the virus is found in all body fluids and skin, making handling of bodies of EVD victims extremely hazardous. In contrast to prevailing biases, bleeding does not occur in all patients and only manifests late in the disease process as bleeding from skin, gums, and the gastrointestinal tract.36 Mortality rate remains high at 50–90% overall with a poorer prognosis seen in those with older age, diarrhea, hemorrhagic conjunctivitis, shortness of breath, confusion/coma, and hemorrhage.37
Patients in early stages of the disease present with the acute onset of flu-like symptoms. Fever is the most common symptom (present in 87%), with fatigue (76%), abdominal pain (44%), and nausea and vomiting (65%) frequently seen, also.37,38,39 Late symptoms are representative of a fulminant infection and SIRS with symptoms of severe vomiting and diarrhea, both of which may be bloody. Other late signs include a coagulopathy identified by diffuse oozing from mucosal surfaces and sites of intravenous lines. Death is often the result of recalcitrant multiorgan system failure.25
Currently there is no vaccine against or pharmacologic treatment for EVD, and the mainstay of therapy is supportive care. Many patients will have severe diarrhea, losing up to 15 L/day and require aggressive resuscitation efforts focused on replenishing circulatory volume. Significant electrolyte abnormalities are common, and correction of these must be done in order to prevent cardiac dysrhythmias. In the early stages of the disease patients can often tolerate oral fluids, antiemetics, and antidiarrheals. Patients with protracted vomiting or in those later stages of the disease should have intravenous fluids administered. Blood transfusions may be necessary, especially for those with hemorrhagic symptoms, and should follow current recommendations for transfusion triggers. Respiratory support in the form of mechanical ventilation may be necessary, but caution should be exercised with noninvasive support, as it may lead to aerosolization.40 Some novel antivirals known to have in vitro or animal anti-Ebola activity were used during the 2014 outbreak, but data regarding their effectiveness are inconclusive at this time. Experimental therapies used during the 2014 EVD outbreak included plasma from convalescent or immune patients and experimental monoclonal antibodies, but it is not clear that either method provided a survival benefit.41,42 Several vaccines are currently undergoing accelerated human trials, but none as yet are commercially available.43
The 2014 EVD outbreak clearly demonstrated how globalization has enhanced the capacity for a previously isolated tropical disease to rapidly spread. Prevention relies on maintaining a level of preparedness of providers and facilities that can receive patients with EVD, provide quality critical care, protect the providers, and assuage the fears of the community. Preventing EVD transmission is divided into mitigating transmission of the primary disease and screening for early identification of the disease as part of planning for a disaster.
Strict adherence to protocols for use of personal protective equipment (PPE) and adoption of practices to limit exposure to body fluids constitute the mainstays of primary prevention. Practiced use of full PPE, as described by the CDC (http://www.cdc.gov/vhf/ebola/healthcare-us/ppe/guidance.html) that is donned and doffed in the presence of a trained observer, is paramount when treating a patient with EVD.44 All practitioners who will come into contact with a patient with EVD should be trained and certified in their ability to properly wear full PPE prior to their first encounter with the patient. The body should be covered from head to toe with single use hood, gown, double gloves, gown (or coveralls), impermeable boot covers, and a respirator or N95 mask. Ideally extended cuff cloves, gowns with thumb hooks, and/or tape securing the gowns and gloves should be used. During contact with the patient, the practitioner should limit contact with surfaces with body fluid, keep their hands away from their face, and employ frequent alcohol-based scrubs on their gloved hands. There should be no rush or shortcuts taken while placing the PPE, so time consideration should be given if plans for procedures or intubation are required. Total time spent in the care of the patient while wearing PPE should be monitored because providers can become fatigued and dehydrated. Elective surgical procedure should be postponed in a patient with EVD and nonoperative alternatives should be strongly considered for urgent conditions (ie, appendicitis, perforated ulcer, etc). A risk-benefit analysis considering the risk of exposure to the operative team must be considered prior to operating for an emergent condition bearing in mind that, in late EVD disease, the patient is unlikely to survive.
Health care preparedness for a real or potential Ebola outbreak mandates the presence of an effective screening procedure that will capture any potential carrier of EVD. A robust program that contains multiple contingency plans and has been rehearsed by all the team members is essential, as disaster leaders should be prepared to operate without significant assistance for at least 72 hours. A simple screening method that can be utilized at any first encounter with a patient (including clerical areas) should focus on the following: (1) recent travel (last 21 days) to an affected area; (2) recent (21 days) direct contact with a patient infected with Ebola.45
Positive responses to these simple questions lead to an escalation of care with an immediate separation and isolation of the patient. After proper isolation, a more focused history identifying exposure risk can be performed. Once a diagnosis of EVD is confirmed, the CDC recommended plans should be in place to ensure immediate isolation is available which includes a private room with a door, a private bathroom, and separate areas for donning and doffing PPE. Other pragmatic plans for handling of lab specimens, environmental waste management, and restriction of nonessential personnel must be in place.46 The institutional management of threatened or actual Ebola outbreak requires trained, professional emergency managers and disaster management experts to be involved in incident command. Incident control should designate a team of site managers who have a constant presence to oversee implementation of safety precautions, monitor adequacy of necessary supplies, and evaluate care in isolation areas.
The high infectious risk and mortality rate of EVD evokes strong emotions of fear, both in healthcare workers and the general public. The incident command should remain the voice of calm and reason during the disaster and encourage constant communication between the front-line providers, the incident commander, and the community.