Immediate Management of Life-Threatening Problems
- Hyperthermia or hypothermia
- Tachycardia
- Tachypnea
- Leukocytosis or leukopenia
- Clinical evidence of infection
Sepsis is a state of systemic inflammation triggered by infection, affecting virtually every organ system. Although the mortality rate from sepsis has been falling, its incidence is increasing and septic shock now accounts for 10% of admissions to ICUs. Septic shock peaks in the sixth decade of life, and factors that can predispose to it include immunodeficiency, cancer, malnutrition, and genetics. Early recognition of sepsis is essential to providing effective care.
The systemic inflammatory response syndrome (SIRS) is characterized by a complicated interplay of multiple inflammatory mediators and may result from trauma, infection, burns, or diseases such as pancreatitis. It is defined as two or more alterations in the following physiologic parameters:
- Body temperature >38°C or <36°C
- Heart rate >90 beats per minute
- Respiratory rate >20, Paco2 <32 mm Hg, or need for mechanical ventilation
- White blood count (WBC) >12,000/mm3 or <4000/mm3, or >10% bands
Sepsis is defined as SIRS with a documented infection, with the identification of microorganisms from a normally sterile fluid or visual inspection of a focus of infection. Severe sepsis consists of sepsis with evidence of end-organ hypoperfusion or dysfunction (eg, prolonged capillary refill, ARDS, mental status changes, or elevated lactate). Septic shock is severe sepsis with persistent hypotension despite adequate fluid resuscitation, with refractory septic shock defined as septic shock requiring high doses of vasopressors.
Provide supplemental oxygen in order to maintain pulse oximetry >92%. Patients with profound mental status changes or hypoxia unresponsive to noninvasive ventilation may require intubation. Early on, arterial blood gas samples may show a respiratory alkalosis, with a metabolic acidosis becoming more prominent as the disease state progresses.
Adequate intravenous access should be obtained early on; consideration should be given to placing a central venous line that will allow monitoring of central venous pressure (CVP) as well as central venous oxygen saturation and allow the rapid infusion of crystalloid. Central venous lines also allow for the prolonged infusion of vasopressors if necessary; norepinephrine and dopamine are first-line agents. Routine use of low-dose (“renal protective”) dopamine is not recommended. An arterial line should be considered for all patients receiving vasopressors.
Traditional clinical measures of perfusion (urine output, capillary refill, tachycardia) may miss hypoperfusion in a significant number of patients. In patients with an elevated lactate >4 or systolic pressure <90, early goal-directed therapy (EGDT) should be considered and aggressive resuscitation with crystalloid should be initiated until a CVP of 8–12 is reached.
EGDT reduces mortality in patients with sepsis. Although not completely clear, treatment should be initiated aggressively in a 6-hour window for optimal results. Patients who meet the SIRS criteria mentioned above and have a suspected infectious etiology along with either a SBP <90 or a lactate >4 mmol/L are candidates for EGDT. Patients should initially be given crystalloid infusion until a CVP of 8–12 is reached. Vasoactive agents are then added to maintain a mean arterial pressure (MAP) greater than 65 mm Hg using either norepinephrine or dopamine. There may be some benefit from addition of low-dose vasopressin in refactory shock. Once the desired MAP is reached, check a mixed venous or central venous oxygen saturation. Those with <70% saturation should be transfused with PRBCs to maintain a hematocrit of at least 30%. Patients with a mixed venous O2 saturation <70% despite an adequate hematocrit should be given inotropic support with dobutamine starting at 2.5 μg/kg/min and titrating to a maximum dose up to 20 μg/kg to improve cardiac output.
In accordance with current guidelines, appropriate antibiotics should be given within the first hour after sepsis is recognized. Remember to obtain needed cultures such as blood, urine, and fluid cultures prior to initiation of therapy, but do not delay treatment for such purposes. Recent literature has suggested that β-lactam monotherapy or later generation cephalosporins such as cefepime are effective and demonstrate equal efficacy compared to β-lactam and aminoglycoside dual therapy without the added nephrotoxicity. Local resistance patterns in the hospital and community as well as the patient’s particular risk for resistant organisms should be considered in antibiotic selection. Gram-positive organisms are now more common as a source for sepsis than gram-negative organisms. Sepsis due to fungal organisms, although carrying a high mortality rate, is rare; routine antifungal coverage is not recommended unless the clinical picture dictates.
When possible, the infectious etiology should be identified and removed surgically. A thorough examination for the source of infection is warranted, particularly in debilitated patients in whom complaints that would prompt evaluation of perineal infection or perirectal abscesses may be absent.
Glycemic control is still encouraged with most sources recommending “moderate” control keeping glucose levels below 150 mg/dL but not in the normal range Corticosteroid therapy has been well researched with most recommendations indicating a “low-dose” steroid approach with no more than 200–300 mg of hydrocortisone per day. This has a higher grade of evidence in patients who fail to respond to a cosyntropin test or have fluid and vasopressor refractory hypotension. Continuation of this low dose and gradual tapering is encouraged. Efficacy regarding recombinant human activated protein C (RhAPC) is still debated but current guidelines continue to recommend RhAPC for patients with an APACHE II score >25 who are at high risk for mortality. Contraindications continue to include recent surgery or other risks for increased bleeding. The presence of disseminated intravascular coagulation (DIC) should not influence the decision to give RhAPC.
Obtain cultures of blood, urine, and sputum if indicated on all patients with severe sepsis. Other sources such as wound, CSF, peritoneal fluid, intravenous catheter sites, and joint fluid may be sent for Gram stain and culture if clinically indicated.
A CBC may show an increased or, more ominously, decreased WBC with evidence of left shift. Thrombocytopenia should prompt evaluation for DIC, with evaluation of fibrinogen and fibrin split products as well as partial thromboplastin (PT) and partial thromboplastin time (PTT). Elevated blood urea nitrogen (BUN) and creatinine may result from renal hypoperfusion, and elevated liver function tests (LFTs) may result from hepatic hypoperfusion. Blood glucose may be increased or decreased, and electrolyte abnormalities are common.
Chest X-ray as well as focused imaging of other potential sources of infection should be pursued as needed.
Vasopressors should only be initiated after adequate fluid resuscitation. Bolus of 20 mL/kg crystalloid should be given initially, with most patients responding after 40–60 mL/kg although larger amounts may be required. Dopamine is the first choice of support for pediatric patients with refractory hypotension despite fluid resuscitation. Patients with low cardiac output and high peripheral resistance may benefit from short-acting vasodilators such as nitroprusside. Infants are at higher risk for hypoglycemia and warrant more frequent monitoring. Blood pressure is not a reliable end point of resuscitation in children as they are able to maintain pressure by peripheral vasoconstriction and increased heart rate to a much greater degree than adults. Hypotension often heralds cardiovascular collapse.
All patients with severe sepsis or septic shock require hospitalization in an ICU.
Those who have acquired their immunodeficiencies at birth or later in life through disease or medical treatment provide the emergency physician with a challenge to both recognize the specific problem and treat it appropriately. Excluding a defect in the skin, our primary host defense, we encounter problems associated with diseases of cell mediated and humoral immunity. In addition, there are infections associated with granulocytes in both function and quantity.
Neutrophils ordinarily make up the majority of circulating WBCs. An absolute neutrophil count below 1000 is clinically significant. Most of these patients have undergone chemotherapy or irradiation. However, acquired neutropenia can come from an untoward response to a drug. The presence of fever >38.5°C, with neutropenia, suggests a related infection. For the evaluation of the source of infection, empiric therapy with admission to the hospital is indicated. Infections with pyogenic organisms such a Staphylococcus aureus and Pseudomonas aeruginosa are common. People with short-term neutropenia have a better prognosis than those chronically affected.
Problems with cell-mediated immunity involve the relationships between tissue macrophages, effector T cells, and cytotoxic T cells. Persons with AIDS, immunosuppression with antirejection drugs or antineoplastic drugs, as well as those with congenital T cell problems suffer from this. What is unique is that they are plagued by infections that are caused by intracellular pathogens. Mycobacteria, cytomegalovirus (CMV), and herpes simplex are a few examples.
It refers to decrease in antibody production or function as well as cytokine production, including pathogen and toxin neutralization, complement activation, and opsonin promotion of phagocytosis. From skin infection and vaginitis to frank sepsis, defects in humoral immunity result in a variety of conditions.
Fever is the most reliable sign of infection in immunocompromised patients and must never be ascribed to an underlying disease until infection has been excluded. In patients with neutropenia with skin and soft tissue infections, there may be lack of abscess formation with persistent redness and pain being the only symptom. A careful evaluation of the lungs, mucous membranes, and the skin may give clues. Because of the relatively low pathogenicity of some of the offending organisms, even infections of the meninges may be subtle.
The CBC is useful in evaluating the immunocompromised patient. With it, the absolute neutrophil count may be estimated by multiplying the percent of observed neutrophils by the total. The usual evaluations of the chest and urine as well as cultures of blood and other fluids will be helpful. Evaluation of the spinal fluid may involve testing for Cryptococcus or CMV, and also staining for AFB.
In febrile patients with granulocyte counts under 1000, antibiotic therapy should be started immediately after material for routine culture has been obtained. Frequently, when the low count has been suspected, the neutropenic patient will have been started on antibiotics by their physician. Antibiotic adsorbing cultures should be used in this case. Circumstances that strengthen the directive for urgent empiric therapy include (1) a rapidly falling granulocyte count, (2) a very low granulocyte count (<500 further increases the risk of infection; <100 is frequently associated with fulminant infection), and (3) other clinical findings suggesting infection.
Current therapy for neutropenic fever varies depending on the illness severity and the “risk classification” of the patient based on disease process and overall health. Current literature identifies successful oral therapy for low risk, otherwise nonseptic, neutropenic patients. Combinations of fluoroquinolones and extended spectrum penicillins have been supported such as ciprofloxacin and amoxicillin/clavulanate.
For high risk or apparently toxic patients, hospital admission and monotherapy are often appropriate. Numerous recent articles support monotherapy, especially with late generation cephalosporins such as ceftazidime and cefepime. Other plausible monotherapy agents include ciprofloxacin and piperacillin–tazobactam. Classical dual therapy combines one of the above with an aminoglycoside such as gentamycin. Patients with risk factors for methicillin-resistant Staph. aureus (MRSA) colonization such as indwelling catheters, skin structure infections, or unknown origin sepsis may have vancomycin added to the regimen until cultures identify an organism.
Neutropenic patients should be hospitalized in private rooms, and strict hand-washing precautions observed. Protective isolation as usually practiced (ie, masks and gowns) does not appear to be effective. Most infections neutropenic patients are derived from their own flora as opposed to infections from other persons and health care providers. This may explain why standard contact isolation procedures are usually minimally effective in preventing infections. Patients should be prescribed a diet free of fresh fruits and vegetables, which are often heavily contaminated with gram-negative bacilli.
All immunocompromised patients with new findings of fever or other signs of infection should be hospitalized.
Emergency Management of Specific Disorders
- Fever
- Nuchal rigidity
- Mental status change
- Photophobia
- Headache
- CSF findings
Meningitis is defined as inflammation of the meninges; it is the major infectious syndrome affecting the CNS. When meningitis is accompanied by parenchymal involvement, it is referred to as meningoencephalitis. The epidemiology of meningitis has changed drastically since Haemophilus influenzae immunizations became available. The incidence of meningitis caused by this agent has decreased by 94%. The average age of meningitis cases peaks in a bimodal fashion. Infants and young adults around the age of 18 are at highest risk in terms of incidence and disease burden. The current mortality according to the Centers for Disease Control (CDC) is 10–14% but with 11–19% of survivors have some permanent neurologic sequelae. Survival depends on prompt recognition and early treatment.
Patients with meningitis present with fever, headache, nuchal rigidity, and mental dysfunction. Seizures and cranial nerve deficits are also common. Infants with meningitis may present with only vomiting, lethargy, irritability, and poor feeding. Elderly patients may present with only low-grade fever and delirium. The headache associated with meningitis is continuous and throbbing and, although generalized, is usually most prominent over the occiput. The pain is increased by jugular vein compression or any other maneuver that increases intracranial pressure (eg, coughing, sneezing, and straining at stool). Neck stiffness and other signs of meningeal irritation must be sought with care because they may not be obvious early and may disappear during coma. Patients with meningitis may be divided into two groups on the basis of the presentation of the disorder.
Symptoms and signs have been present for less than 24 hours and are rapidly progressive. The causative organisms are usually pyogenic bacteria, and the mortality rate is approximately 50%.
Symptoms and signs have been present for 1–7 days. Meningitis is due to bacteria, viruses, or fungi, and the death rate due to bacterial infection is much lower than in patients with acute presentation of disease. Aseptic meningitis is typically caused by viruses (enteroviruses, herpes simplex virus [HSV], or Epstein–Barr virus). Suggestive features such as respiratory tract syndrome and hand–foot–mouth syndrome strengthen the diagnosis. Chronic meningitis is defined as meningitis present for more than 4 weeks; the major infectious causes are tuberculous meningitis and cryptococci.
Perform lumbar puncture immediately in the absence of papilledema and focal neurologic findings. For contraindications to lumbar puncture, see Table 42–1. Interpretation of CSF findings is shown in Table 42–2. Draw blood for serum glucose measurement and for culture. Gram staining of CSF will allow presumptive identification of the causative agent. Even if no organisms are seen on Gram-stained smears of CSF, bacterial meningitis is a likely diagnosis and warrants empiric antimicrobial therapy if total CSF leukocytes number more than 1000, if polymorphonuclears (PMNs) make up at least 85% of the white cells in CSF, or if the CSF glucose is less than 50% of the serum glucose level in a simultaneously drawn blood sample. The differential diagnosis in patients in whom PMNs are less than 85% of the CSF white count must include several possible causes of acute lymphocytic meningitis (Table 42–3). Prior treatment with antibiotics could result in sterile cultures of CSF.
|
Measure | Normal | Bacterial Meningitis | Viral Meningitis | Fungal Meningitis | Tuberculous Meningitis | Abscess |
---|---|---|---|---|---|---|
WBC/mL | 0–5 | >1000 | <1000 | 100–500 | 100–500 | 10–1000 |
PMNs (%) | 0–15 | >80 | <50 | <50 | <50 | <50 |
Lymphocytes (%) | >50 | <50 | >50 | >80 | Increased monocytes | Variable |
Glucose | 45–65 | <40 | 45–65 | 30–45 | 30–45 | 45–60 |
CSF–blood glucose ratio | 0.6 | <0.4 | 0.6 | <0.4 | <0.4 | 0.6 |
Protein | 20–45 | >150 | 50–100 | 100–500 | 100–500 | >50 |
Pressure | 6–20 | >25–30 | Variable | >20 | >20 | Variable |
|
When bacterial meningitis is suspected, begin administration of appropriate empiric antibiotics immediately (Table 42–4). Give the first dose as soon as samples of CSF and blood have been collected for tests; the goal is to begin intravenous administration of antimicrobials within 30 minutes after a patient with acute presentation of meningitis has sought treatment. If lumbar puncture must be delayed for computed tomography (CT) scan, obtain two blood samples for culture and begin appropriate antimicrobials. Perform lumbar puncture after mass lesion has been excluded and obtain CSF for microscopic examination as soon as possible. For pathogen-specific antibiotic therapy for bacterial meningitis, see Table 42–5.
Treatment is based on results of Gram staining of CSF and other tests. If meningitis is likely but Gram staining is negative, begin empiric treatment based on the patient’s clinical characteristics pending the results of CSF studies.
In patients thought to have a brain abscess, begin intravenous therapy with a combination of penicillin and metronidazole or a third-generation cephalosporin. Obtain an emergency CT scan.
Age | Major Pathogens | Antibiotic Regimen | Alternative Regimens | Comment |
---|---|---|---|---|
Less than 3 months | Group B streptococci, Listeria monocytogenes, Escherichia coli, Strep. pneumoniae | Ampicillin plus ceftriaxone (or cefotaxime) | Chloramphenicol plus gentamicin | CSF levels are not reliable in low-birth-weight infants and should be monitored |
3 months–18 years | Neisseria meningitidis, S. pneumoniae, Haemophilus influenzae | Ceftriaxone (or cefotaxime) | Meropenem or Chloramphenicol | Add vancomycin in areas with greater than 2% incidence of highly drug resistant S. pneumoniae |
18–50 years | S. pneumoniae, N. meningitides, H. influenzae | Ceftriaxone (or cefotaxime) | Meropenem or chloramphenical | Add vancomycin in areas with greater than 2% incidence of highly drug resistant S. pneumoniae |
50 years and older | S. pneumoniae, L. monocytogenes, gram-negative bacilli | Ampicillin plus ceftraxone (or cefotaxime) | Ampicillin plus fluoroquinolone (ciprofloxacin, levofloxacin) | Add vancomycin in areas with greater than 2% incidence of highly drug resistant S. pneumoniae; for patients who have major penicillin allergy, TMP-SMZ can substitute for ampicillin to treat L. monocytogenes infection |
Organism | Preferred Regimen | Alternative Choices | Duration (days) |
---|---|---|---|
Group B streptococci | Penicillin G (or ampicillin) | Vancomycin | 14–21 |
Haemophilus influenzae | Ceftriaxone (or cefotaxime) | Chloramphenicol | 7–10 |
Listeria monocytogenes | Ampicillin plus gentamicin | TMP-SMZ | 14–21 |
Neisseria meningitidis | Penicillin G (or ampicillin) | Ceftriaxone (or cefotaxime); chloramphenicol | 7–10 |
Strep. pneumoniae (MIC <0.1) | Ceftriaxone (or cefotaxime) | Penicillin; meropenem | 10–14 (MIC <0.1) |
S. pneumoniae (MIC <0.1) | Vancomycin plus ceftriaxone (or cefotaxime) | Substitute rifampin for vancomycin; use vancomycin monotherapy if patient is highly allergic to cephalosporins | 10–14 |
Studies have failed to clearly define the utility of corticosteroids in the patient with bacterial meningitis. However, evidence does suggest a potential benefit and no prominent negative effects. Therefore, use is recommended, especially with S. pneumoniae meningitis in adults and in children older than 2 months. Dexamethasone 10 mg should be administered to adults preferably prior to, or along with antibiotics. Utilization after antibiotic administration has been found not to be helpful.
General supportive care measures should be started in the emergency department. Protect the patient’s airway, and provide padded rails or restraints for agitated or delirious patients. If seizures occur, begin anticonvulsant therapy. Avoid overhydration, which may worsen cerebral edema.
Immediate hospitalization is warranted for all patients, except those with aseptic (viral) meningitis who appear well and can be observed at home.
- Grunting, tachypnea
- Focal lung exam
- Radiographic findings
The early neonatal period, birth to 2 weeks, is dominated by group B Streptococcus, Listeria, and gram-negative Escherichia coli and Klebsiella pneumoniae. These are acquired at birth. These infants will have poor feeding, paradoxical irritability, grunting, and tachypnea. Cough may only be an infrequent feature. Sepsis or meningitis may accompany the pneumonia.
A total sepsis workup is clearly indicated for these infants. Laboratory findings will vary, but the diagnosis will be confirmed with the chest X-ray.
Appropriate antibiotic therapy is outlined in Table 42–6. All neonates should be hospitalized.
Age Group | Cause | Primary Treatment | Alternative Treatment |
---|---|---|---|
Neonates |
|
|
|
1–3 months |
|
| Cefuroxime |
3 months to 5 years |
|
|
|
5 years to 18 years |
| Macrolide |
|
In infants over 2 months of age, more classic signs and symptoms of pneumonia are present but tachypnea predominates. Cough, grunting, rales, and wheezing may be seen and fever is variable.
As viruses predominate this age group, an elevation of the WBC above 15,000/mm3 is suggestive but not diagnostic for bacterial infection. Arterial blood gas analysis may be obtained to assess the adequacy of ventilation. Electrolyte levels and BUN are useful in assessing the degree of dehydration, the most frequent complication seen in this age group. Obtaining sputum is difficult without direct tracheal aspiration, or pneumocentesis. Blood cultures though frequently obtained are rarely positive as H. influenzae and S. pneumoniae have become rarer. Indirect identification of respiratory syncytial virus (RSV) and influenza have been very helpful in confirming the etiology of the pneumonia.
Appropriate antibiotic therapy should be guided by age and is outlined in Table 42–6. Severely ill infants (ie, with respiratory distress, hyperthermia, or Po2 <70) should be hospitalized.
Infection with Mycoplasma pneumoniae begins to predominate. Cough rales and wheezing may be seen. Bullous myringitis helps confirm the etiology and thus tailor appropriate treatment. Fever is very common with pneumonia in this age group, while cough may be present, abdominal pain may be the child’s chief complaint.
In pneumonia due to M. pneumoniae, the white cell count is usually normal or slightly elevated, and chest X-ray reveals scattered segmental infiltrates, atelectasis, interstitial disease, or, less frequently, lobar consolidation.
In pneumonia due to bacteria other than M. pneumoniae, the white cell count usually exceeds 15,000. Chest X-ray abnormalities include patchy infiltrates, increased bronchovascular markings, lobar consolidation, cavitary infiltrates, and pleural effusions or empyema. Gram-stained smears of sputum may allow for a presumptive diagnosis if numerous PMNs, few epithelial cells, and a predominant microorganism are found. Pleural fluid should be examined if present.
Appropriate antibiotic therapy is outlined in Table 42–6. Hospitalization is indicated for patients with pneumonia who require oxygen or have intractable vomiting. In addition, patients with preexisting pulmonary disease and all patients with bilateral bacterial pneumonia should be hospitalized.
Complete CDC data from 2006 indicates pneumonia and respiratory infection to be the 8th leading cause of death in the United States. Over 1.2 million patients were admitted with pneumonia with an average of 5.1 days hospital stay. This contributes to a multibillion dollar cost related to pneumonia care. S. pneumoniae remains the most common cause of community-acquired pneumonia (CAP) in the adult population, with atypical organisms such as M. pneumoniae and Chlamydiapneumoniae common in young adults. Patients with structural lung disease, the elderly, nursing home residents, alcoholics, those with recent antibiotic exposure, and those who are immunosuppressed (>10 mg/d of prednisone) or have recently been hospitalized are more likely to be infected with resistant S. pneumoniae or gram-negative organisms. Influenza, varicella, and RSV (particularly in nursing home residents) are common viral causes of CAP.
Atypical or viral pneumonias may develop insidiously with focal respiratory complaints preceded by a 3- to 5-day history of malaise, fever, myalgias, and sore throat. Auscultation of the lungs typically reveals diffuse findings such as wheezing or fine rales, which may be slightly more prominent in the lung bases. Bacterial pneumonias are characterized by an abrupt onset of fever, chills, cough often productive of purulent or blood-tinged sputum, and pleuritic chest pain. Physical examination reveals a focal area of rales and possible consolidation. Legionella pneumonia presents as a severe form of lobar pneumonia and is classically associated with diarrhea. The diagnosis of pneumonia in nursing-home residents requires a high index of suspicion as they often have nonspecific presentations, often in the absence of cough, fever, and dyspnea. Aspiration pneumonia is more common in the elderly, those with poor dentition, and alcoholics, and is characterized by very foul-smelling sputum.
A chest X-ray should be obtained to confirm the diagnosis of pneumonia, help guide initial treatment, and exclude other etiologies. Chest X-ray findings with the associated organisms are outlined in Table 42–7. A right lower lobe or right upper lobe infiltrate in the setting of aspiration may represent aspiration pneumonitis rather than pneumonia if other clinical indicators of infection are absent. CT may be helpful in differentiating between lung abscess and empyema when the chest X-ray is equivocal. An oxygen saturation should be obtained on all patients with an arterial blood gas reserved for severely ill patients. Gram staining and culture of the sputum is the most valuable study for patients in whom it is important to determine an etiology (critically ill, those at risk for resistant organisms). Urinary antigen testing for Legionella pneumophila and S. pneumoniae is more sensitive at detecting infection with these organisms than are blood cultures but provides no data on antibiotic sensitivity. In patients younger than 50 years with no significant comorbidities, who are not hypoxic, and who do not have any of the abnormal physical examination findings, no further laboratory testing may be needed. Leukocytosis is a common but nonspecific finding, while leukopenia in the setting of clinical infection is often ominous. Elderly patients commonly show prerenal azotemia, and hyponatremia with elevated LFTs are associated with Legionella pneumonia.
Finding | Description | Associated Organisms |
---|---|---|
Lobar consolidation | Nonsegmental, homogenous consolidation involving one lobe; may have air bronchograms |
|
Bronchopneumonia | Peribronchial thickening, poorly defined air space opacities (“patchy” consolidation) |
|
Interstitial pneumonia | Edema and infiltrate in alveolar septa, surrounding small airway/vessels |
|
Abscess | Air–fluid level, often with adjacent parenchymal consolidation |
|
Effusion | Assumes shape of pleural space; if air–fluid level present, longer on lateral view | Any; more common in severe pneumonia ~10% S. pneumoniae; almost 50% of L. pneumophila and H. influenzae |
Pneumatocele | Thin-walled, gas-filled spaces within parenchyma | Present in up to 50% S. aureus pneumonias in children |
Initial treatment is empiric and based on the presumed causative organism for the patient’s clinical presentation. Hospitalized patients should be divided into one of three categories: CAP, health care associated pneumonia (HCAP) early or with no risk factors for multidrug resistant pathogens (MDR), and HCAP late or with risk factors for MDR (Table 42–8).
Community-acquired pneumonia (CAP)—No recent contact with health care system or hospital admissions in past |
Health care associated pneumonia, early/low-risk (HCAP)—Includes patients within 5 days of hospital admission to non-ICU setting, not intubated. Otherwise not meeting multi drug resistant (MDR) pathogen risk below. |
Health care associated pneumonia, late/MDR risk (HCAP)—Includes patients with the following risk factors:
|
Recommended empiric antibiotic regimens for both CAP and HCAP are listed in Table 42–9. Current literature reviews have failed to demonstrate any statistically significant research demonstrating higher therapeutic success with any one outpatient regimen for CAP. Prompt recognition and treatment with a variety of agents as initial therapy seem appropriate. Although coinfection with atypical organisms is common, it is not clear whether adding atypical coverage is beneficial in younger patients. Initial enteral treatment recommendations include macrolides as a common first-line choice with amoxicillin/clavulanate and doxycycline cited as appropriate other choices. Respiratory fluoroquinolones are commonly second-line therapy for failed treatment or high-risk patients and should probably be reserved for this use.
Age Group | First-Line Treatments | Alternative Treatment |
---|---|---|
CAP (not hospitalized) |
|
|
CAP (hospitalized medical bed) | Respiratory fluoroquinolonea |
|
CAP (hospitalized ICU bed) |
|
|
HCAP (not admitted) | Respiratory fluoroquinolonea |
|
HCAP Early/Low-Risk MDR | Ceftriaxone or Respiratory fluoroquinolonea | Ampicillin/sulbactam |
HCAP Late/MDR Risk |
|
|
Aspiration | Clindamycin | Amoxicillin–clavulanate, imipenem, meropenem |
Hospitalized patients should be treated with a β-lactam agent and macrolide or a fluoroquinolone as monotherapy, with consideration given to resistant organisms and appropriate gram-negative coverage, particularly for ICU patients. Administration of antibiotics rapidly following presentation and diagnosis is critical. Although classically the standard goal for administration of parenteral antibiotics has been 4 hours, data has shown that time periods up to 6 hours may still be acceptable. Clearly earlier administration is preferable and decreases mortality, even if the diagnosis remains unclear and the initial antibiotic regimen may not be optimal.
The use of validated scoring systems such as the Pneumonia PORT Severity Index has been demonstrated to determine effectively that patients may be safely treated on an outpatient basis (see Table 42–10). Classes I, II, and III (≤ 90 points) patients are at sufficiently low risk for death that they can be considered for outpatient treatment or an abbreviated course of inpatient care. Class IV and V patients should be hospitalized.
Characteristic | Points Assigned |
---|---|
Age | |
Men | Age |
Women | Age—10 |
Nursing Home Resident | +10 |
Coexisting Illnesses | |
Neoplastic disease | +30 |
Liver disease | +20 |
CHF | +10 |
Cerebrovascular disease | +10 |
Renal disease | +10 |
Physical Examination Findings | |
Altered mental status | +20 |
Respiratory rate ≥30/min | +20 |
SBP <90 mm Hg | +20 |
Temperature <35 or > 40 | +15 |
Pulse ≥125/min | +10 |
Laboratory/X-Ray Findings | |
Arterial pH <7.35 | +30 |
BUN >30 mg/dL | +20 |
Sodium <130 mmol/L | +20 |
Glucose ≥250 mg/dL | +10 |
Hematocrit <30% | +10 |
Pao2 <60 mm Hg | +10 |
Pleural effusion | +10 |
Risk Group (# of points) | Mortality |
I (pts not calculated) | 0–0.4% |
II (≤70) | 0.4–0.7% |
III (71–90) | 0–2.8% |
IV (91–130) | 8.2–9.3% |
V (>130) | 27–31.1% |
- Wheezing
- Cough
- Low-grade fever
- Tachypnea
Bronchiolitis is an acute inflammation of the bronchioles, most commonly resulting from a viral infection. It typically affects children from birth to age 2 years and occurs mostly during the winter months (November to March). RSV is the cause in 60–90% of cases; the remaining cases are caused by parainfluenza, adenovirus, rhinovirus, and influenza and human Bocavirus.
The child with bronchiolitis typically has a 4-day history of clear profuse rhinorrhea and congestion, usually accompanied by low-grade fever followed by the development of a cough, tachypnea, and wheezing. Signs of respiratory distress including cyanosis and accessory muscle use may be evident, and inspiratory wheezing and crackles are typically heard on auscultation of the patient’s lungs. Apnea can occur, and approximately 2–7% of children ill enough to require hospitalization develop respiratory failure, and require intubation.
A nasopharyngeal aspirate can be sent for rapid identification of RSV and influenza and have become the standard for diagnosis. A positive test does not preclude the diagnosis of asthma that is also an inflammatory process. A chest X-ray is recommended for all patients who do not already have chronic respiratory problems and may show findings characteristic of bronchiolitis: hyperinflation, atelectasis, peribronchial thickening, and diffuse interstitial infiltrates.
Oxygen rapidly relieves hypoxemia and is the most important therapeutic agent for bronchiolitis. A trial of bronchodilators is indicated. Studies evaluating the use of glucocorticoids show no improvement in outcome, provided that asthma can be excluded. Ribavirin is a synthetic nucleoside analogue that has virostatic activity against RSV and is recommended for use in patients with a history of congenital heart disease or chronic lung disease, preterm infants, infants younger than 6 weeks, and infants ventilated for RSV infection.
Criteria suggestive of severe disease include the following: ill or toxic appearing, oxygen saturation less than 95%, gestational age less than 34 weeks, respiratory rate greater than 70 breaths/min, atelectasis on X-ray, and age less than 3 months. The infant’s oxygen saturation while feeding is the single best objective measure of severe disease.
- Fever
- Painful joint
- Joint effusions
- Arthrocentesis findings
Left untreated, septic arthritis rapidly destroys articular cartilage, causing permanent joint damage. Delay between the onset of symptoms and treatment is the major determining factor for prognosis. Joint infection may occur by hematogenous route, direct inoculation, or spread of contiguous infections. Hematogenous infection in children was the most common route, but HIB immunization has decreased this significantly. The peak incidence occurs in children under age 3 years, and boys are affected twice as often as girls. However, with the increasing frequency of prosthetic joints, a new group has emerged that may be the most problematic.
Septic arthritis typically affects only one or a few asymmetrically distributed joints. Because joint infection superimposed on rheumatoid arthritis sometimes occurs, any joint that develops inflammation out of proportion to that in other affected joints should be aspirated to rule out the possibility of infection in patients with rheumatoid arthritis. There are about 20,000 cases of septic arthritis in the United States annually with gonococcus being the leading cause and Staph. aureus in second place. People with existing joint damage from rheumatoid arthritis and surgery are at risk. Other groups at high risk include intravenous drug abusers and patients on hemodialysis. Aspiration of the affected joint in the emergency department is often necessary to differentiate septic arthritis from other causes of synovitis, such as gout or pseudogout.
Patients with septic arthritis usually have acute or subacute onset of pain, erythema, swelling, and limitation of motion in the affected joints. The patients most likely will show signs of systemic infection with fever chills and an ill appearance. The arthritis more commonly affects the large joints, especially the knee. In infants or neonates, failure to feed or pseudoparalysis of the extremity may be present.
Definitive diagnosis is established by demonstration of the infecting organism in synovial tissue or joint fluid. Blood cultures may be positive even though cultures of joint fluid are negative and should be obtained for all patients thought to have septic arthritis.
Joint fluid typically shows high leukocyte counts, usually over 50,000, although the count may not be strikingly elevated in early disease. Synovial fluid should be considered inflammatory and possibly infectious if the count is above 7500. The higher the white cell count in joint fluid, the greater the likelihood of bacterial or fungal arthritis. The glucose content of synovial fluid is usually lower than normal but occasionally may be normal. If no antimicrobial therapy has been given, smears and cultures often reveal the causative organism. A synovial fluid lactic acid test may be useful in excluding septic arthritis; the test has a negative predictive value of 97%. Results of other laboratory tests are variable, and plain X-rays of affected joints are usually negative early in the disease.
In gonococcal arthritis, Gram-stained smears and cultures of joint fluid are negative in 50–75% of cases, although in 86% of patients, cultures of exudates from the cervix, urethra, pharynx, or rectum demonstrate gonococci. Because the gonococcus is a fastidious organism, demonstration of its growth in cultures depends on prompt processing of specimens by the laboratory. Because special handling is also required, all specimens submitted should bear the instruction “Rule out gonorrhea.” Prompt response to antimicrobial therapy helps confirm the diagnosis of gonococcal arthritis.
Aspirate affected joints. Aspiration is necessary except for infections in inaccessible joints. Open drainage is almost never required in gonococcal arthritis.
High doses of intravenous antibiotics should be given (Table 42–11). Intra-articular instillation of antibiotics is unnecessary because high antibiotic levels are attained in synovial fluid when drugs are given intravenously. If no organisms are seen on Gram-stained smears of synovial fluid, but other findings suggest septic arthritis, empiric antibiotic therapy based on the type of patient and clinical findings should be started depending on the results of culture and sensitivity.
Age Group | Cause | Primary Treatment | Alternative Treatment |
---|---|---|---|
Infant (<3 months) |
| Antistaphylococcal penicillin + third-generation cephalosporin | Antistaphylococcal penicillin + aminoglycoside |
Children (3 months–14 years) |
| Antistaphylococcal penicillin + third-generation cephalosporin | Vancomycin + third-generation cephalosporin |
Adults (acute monoarticular; sexually active) | N. gonorrhoeae | Ceftriaxone or cefotaxime or ceftizoxime | Nafcillin if gram-positive organisms are found |
Adults (acute monoarticular; not sexually active) |
| Antistaphylococcal penicillin + third-generation cephalosporin | Antistaphylococcal penicillin + ciprofloxacin |
Adult (polyarticular) | N. gonorrhoeae | Ceftriaxone |
Hospitalize all patients with suspected or documented septic arthritis.
- Pain, fever
- Increased erythrocyte sedimentation rate
- Biopsy findings
Osteomyelitis is an infection of bone that affects all age groups. The infecting organisms are bacteria, mycobacteria, or fungi. For purposes of discussion, osteomyelitis can be classified according to the pathogenic mechanism: (1) hematogenous osteomyelitis and (2) osteomyelitis secondary to contiguous focus of infection. Hematogenous osteomyelitis is common in children, although its incidence is increasing in older age groups. Hematogenous osteomyelitis in adults usually involves the vertebral bodies. Spread of disease from a contiguous focus of infection is the most common pathogenic mechanism in adults. In both children and adults, the most commonly involved bones are the long bones, especially those of the lower extremities; this is particularly true in children. Orthopedic procedures or traumatic wounds predispose to osteomyelitis of the extremities. Sometimes a third classification of osteomyelitis from peripheral vascular disease is included, but this is likely a predisposing condition to contiguous spread.
The abrupt onset of high fever, systemic toxicity, and physical findings of local suppuration surrounding the involved bone (local pain, swelling, and tenderness) are typical. The disease may be more indolent, particularly in patients with vertebral osteomyelitis. Patients with vertebral osteomyelitis may have low-grade or intermittent fever or back pain that may be either severe or only nagging and may not cause extreme discomfort or immobility until late in the disease. Focal tenderness over the dorsal spines of the involved vertebral bodies may be the only physical finding.
The most common predisposing factor is postoperative infection, such as that following open reduction in fractures. Extension of soft tissue infections to bone from infected fingers and toes, infected teeth, or infected sinuses also occurs. Most patients are over age 50 years and may present with fever, swelling, and erythema in the initial episode. During recurrences, sinus formation and drainage are the major presenting signs.
Patients with osteomyelitis associated with vascular insufficiency invariably have diabetes mellitus or severe peripheral vascular disease. The toes and small bones of the feet are usually affected. Local signs and symptoms such as pain, swelling, redness, or frank cellulitis with deep ulcers in the soft tissue are prominent. Pain is often absent because of diabetic neuropathy.
Routine laboratory tests are of limited value in the diagnosis of osteomyelitis. The leukocyte count is often elevated in acute disease but may be normal in more chronic infection. The erythrocyte sedimentation rate and C-reactive protein are elevated in most patients. Radiographic procedures are the primary diagnostic tool, although plain X-rays may not show signs of disease until 10–14 days after symptom onset. The earliest visible X-ray changes are adjacent soft tissue swelling and periosteal reaction. Lytic lesions and areas of sclerosis may then develop. If osteomyelitis is suspected and plain X-rays fail to reveal signs of disease, MRI or bone scan should be performed. The diagnosis is confirmed by culture and histologic examination of bone. Bacteriologic findings vary, and cultures should be obtained from bone (via needle aspiration or surgical biopsy) or blood (results are positive in 50% of cases in patients with acute hematogenous osteomyelitis).
The most important therapeutic measures are systemic antibiotics and surgery to drain abscesses or for debridement of necrotic tissue. The selection of an antibiotic depends on identification of the causative organism. If the disease is uncomplicated (ie, involves a long bone in a patient without underlying medical problems), if the patient is a child, or if the patient is critically ill, then antistaphylococcal therapy should be initiated because Staph. aureus is the most common infective organism.
Surgery in acute osteomyelitis should be limited to biopsy for diagnosis, drainage of suppurative areas, and debridement of necrotic bone. Surgical drainage is also indicated if neurologic abnormalities are present or develop in patients with vertebral or cranial osteomyelitis or if infection spreads to the hip joint in a child.
Patients with acute osteomyelitis should be hospitalized for intravenous antimicrobial therapy.
- Sore throat
- Fever
- Erythematous pharynx
- Odynophagia
Acute pharyngitis is a common presenting complaint, particularly in the winter months, and is caused by a multitude of organisms (see Table 42–12