Infectious Disease Emergencies

General Considerations

• Acutely ill infected febrile pts requiring emergent attention must be appropriately

evaluated and treated at presentation to improve outcome. The physician

should quickly assess general appearance to gain a subjective sense of whether

the pt is septic or toxic.

• History: The physician should assess:

Onset and duration of symptoms, changes in severity or rate of progression

over time

Host factors (e.g., alcoholism, IV drug use) and comorbid conditions

(e.g., asplenia, diabetes)

Potential nidus for invasive infection (e.g., URI or influenza, trauma,

burn, foreign body) Exposure history (e.g., travel, pets, diet, medication use, sick contacts,

menstruation history, sexual contacts)

• Physical examination

General appearance (e.g., agitation or lethargy, vital signs)

Special attention to skin and soft tissue examination, neurologic examination,

assessment of mental status

• Diagnostic workup

Bloodwork: cultures, CBC withdifferential, electrolytes, renal function

tests, LFTs, blood smear examination, buffy coat

CSF cultures if meningitis is possible. Withfocal neurologic signs, papilledema,

or abnormal mental status, obtain blood cultures, begin antibiotics,

perform brain imaging, and then consider LP.

CT or MRI to evaluate focal abscesses; cultures of wounds or scraping

of skin lesions as indicated. No diagnostic procedure should delay treatment

for more than minutes.

• Treatment

See Table 26-1. Urgent surgical attention may be indicated.

Specific Presentations (Table 26-1)

Sepsis without an Obvious Focus of Primary Infection Nonspecific

symptoms and signs progressing rapidly to hypotension, tachycardia, tachypnea,

altered mental status, and/or DIC

1. Septic shock: primary site not initially identified, bacteremia and shock

evident

2. Overwhelming infection in asplenic pts

a. The risk of severe sepsis remains increased throughout life, but 50–

70% of cases occur in the first 2 years after splenectomy.

b. Streptococcus pneumoniae is the most common etiologic agent, with

mortality rates up to 80%.

3. Babesiosis: history of travel to endemic areas, tick bite 1–4 weeks previously

a. Asplenia and age _60 years are risk factors for severe disease.

b. Babesia microti is transmitted by Ixodes scapularis, the tick that also

transmits Borrelia burgdorferi (Lyme disease) and ehrlichiae. Co-infections

can result in more severe disease.

c. European strain, B. divergens, causes more fulminant disease.

d. Symptoms are nonspecific fever, chills, anorexia, headache, myalgias

that can progress to hemolysis, jaundice, and renal and respiratory failure.

4. Other sepsis syndromes

a. Tularemia (associated withwild rabbit, tick, and tabanid fly contact)

and plague (associated withcontact withsquirrels, prairie dogs, chipmunks);

also category A agents of bioterrorism

b. Mortality rates for typhoidal or septic forms of these infections are

_30%.

Sepsis with Skin Manifestations

1. Maculopapular rashes: usually not emergent but seen in early meningococcemia

and rickettsial disease. Primary HIV infection can present withrash ;

early recognition and treatment can improve prognosis.

2. Petechiae

a. Meningococcemia: young children at greatest risk; outbreaks in

schools and army barracks

Headache, nausea, myalgias, altered mental status, meningismus

Petechiae begin at ankles, wrists, axillae, and mucosal surfaces and

progress to purpura and DIC.

Mortality rates exceed 90% among pts without meningitis, with

rash, hypotension, and normal/low WBC count and ESR.

b.Rocky Mountain spotted fever: history of tick bite and/or travel or

outdoor activity

Headache, malaise, myalgias, nausea, vomiting, anorexia

By day 3, blanching macules that become hemorrhagic, starting at

wrists and ankles and spreading to legs and trunk, then palms and soles

Hypotension, noncardiogenic pulmonary edema, confusion, lethargy,

encephalitis, coma in progressive disease

c.Purpura fulminans: cutaneous manifestation of DIC; large ecchymotic

areas and hemorrhagic bullae; associated with CHF, septic shock, acute

renal failure, acidosis

3.Ecthyma gangrenosum: hemorrhagic vesicles with central necrosis and ulceration

in septic shock with Pseudomonas aeruginosa or Aeromonas hydrophila

4.Other emergent infections associated with rash

a. Vibrio vulnificus and other noncholera vibrios: bacteremic infections

and sepsis after contaminated shellfish ingestion, typically in hosts with

liver disease.Skin findings: lower-extremity bullous or hemorrhagic

lesions

b. Capnocytophaga canimorsus: septic shock in asplenic pts, typically

after dog bite.Skin manifestations: exanthem, erythema multiforme,

peripheral cyanosis, petechiae

5.Erythroderma: diffuse sunburn-like rash that desquamates after 1–2 weeks;

hypotension; multiorgan failure; renal failure (may precede hypotension)

a. Staphylococcus aureus toxic shock syndrome (TSS): usually no primary

focal infection, colonization of vagina or postoperative wound,

5–15% mortality

b.Streptococcal TSS: less frequent desquamation, 30–70% mortality

Sepsis with a Soft Tissue/Muscle Primary Focus

1.Necrotizing fasciitis

a.Can arise at site of minimal trauma, postoperative incision, varicella

b.Risk factors: diabetes, peripheral vascular disease, IV drug use, NSAID

use in setting of soft tissue infection

c.Bacteremia, hypotension, physical findings minimal compared to degree

of pain, fever, toxicity; infected area red, hot, shiny, exquisitely

tender

d.Progression to bullae, necrosis; decrease in pain due to peripheral nerve

destruction an ominous sign

e.Mortality: 100% without surgery, 70% in setting of TSS, 30% overall

2.Clostridial myonecrosis

a.Either secondary to trauma or surgery or spontaneous (associated with

Clostridium septicum infection and underlying malignancy)

b.Massive necrotizing gangrene, toxicity, shock, death within hours

c.Pain and toxicity out of proportion to physical findings. Pts are

apathetic, tachycardic, and tachypneic, with a sense of impending

doom.

d.Mottled, bronze-colored overlying skin or bullous lesions; drainage

with mousy or sweet odor; crepitus

e.Mortality: 12% (extremity myonecrosis) to 63–65% (trunk or spontaneous

myonecrosis)

Neurologic Infections with or without Septic Shock

1.Bacterial meningitis

a.Classic triad of headache, meningismus, and fever in one-half to twothirds

of pts

Blood cultures positive in 50–60% of pts

c. Mortality associated withcoma, respiratory distress, shock, CSF protein

_2.5 g/L, peripheral WBC count _5000/_L, serum Na level

_135 mmol/L

2. Brain abscess

a. Often without systemic signs, can present as space-occupying lesion

b. Headache, focal neurologic signs, papilledema

c. From contiguous foci or hematogenous infection (e.g., endocarditis)

3. Spinal epidural abscesses

a. Risk factors: diabetes, IV drug use, chronic alcohol use, spinal trauma

or surgery, epidural anesthesia

b. Thoracic or lumbar spine most common sites

c. Back pain, neurologic deficits, fever, elevated ESR and WBC counts

Focal Syndromes with a Fulminant Course

1. Rhinocerebral mucormycosis

a. Risk factors: diabetes, malignancy

b. Low-grade fever, dull sinus pain, diplopia, decreased mental status,

chemosis, proptosis, hard-palate lesions that respect the midline

2. Acute bacterial endocarditis

a. Risk factors: malignancy, diabetes, IV drug use, alcoholism

b. Rapid onset, changing murmur, CHF

c. Rapid valvular destruction, pulmonary edema, hypotension, myocardial

abscesses, conduction abnormalities and arrhythmias, large friable

vegetations, major arterial emboli withtissue infarction

3. Inhalational anthrax: Bacillus anthracis, category A agent of bioterrorism

a. Malaise, fever, cough, nausea, sweats, shortness of breath, headache

b. CXR: mediastinal widening, pulmonary infiltrates, pleural effusions