Cellulitis is a spreading acute infection of the skin and subcutaneous tissues
characterized by erythema, warmth, swelling, and tenderness. It may be
classified as mild and uncomplicated, severe, high risk, or necrotizing.
Etiology and Clinical Features
Most cases of cellulitis are mild and uncomplicated.
They are caused by group A streptococci or Staphylococcus aureus. Diffuse erythema,
swelling, and tenderness develop over 2 to 4 days. In an extremity, a red line
along the course of lymphatic vessels indicates accompanying lymphangitis.
Enlargement and tenderness of regional lymph nodes are common. Fever, malaise,
and chills often are present.
Orbital cellulitis is a rare complication of sinusitis and carries a risk of
blindness, brain abscess, and meningitis. Erysipelas usually follows a
streptococcal sore throat and usually affects the young and the elderly. The
infection involves the dermis and the lymphatic vessels and manifests as pain
and bright-red peau d'orange lesions with advancing red borders that are
sharply demarcated from normal skin. Erysipeloid is a form of cellulitis that
occurs among workers who handle fish, meat, and poultry. It is caused by the
gram-positive bacillus Erysipelothrix rhusiopathiae. About 1 week after a minor
injury to the hand, a violaceous painful area appears. As the central area
clears, the lesion spreads outward with distinct raised borders. Animal and
human bites of the hands are potentially dangerous because of tissue damage and
secondary infection. Pasteurella multocida often infects dog and cat bites, and
Eikenella corrodens often is implicated in human bites. Deep infections such as
tenosynovitis are particularly common after human bites. Necrotizing cellulitis
is a serious gangrenous soft-tissue infection often associated with the
presence of anaerobic bacteria, tissue toxins, and bacterial synergy. It should
be suspected when a patient has edema out of proportion to erythema, skin
vesicles, crepitus on palpation or air in the tissues
on a radiograph, local anesthesia, or patchy gangrene of the skin.
Most cases of cellulitis can be managed simply on an
outpatient basis. Severe, complicated, or high-risk infections necessitate
aggressive inpatient antibiotic therapy and often surgery. Patients with
necrotizing infections must be treated surgically. Uncomplicated mild
cellulitis, commonly caused by Streptococcus pyogenes or S. aureus, responds
well to oral cloxacillin or cephalexin (500 mg every 6 hours for 7 to 10 days).
For patients allergic to penicillin, erythromycin (500 mg every 6 hours for 7
to 10 days) is an alternative. Local therapy includes cleansing the area and
resting the extremity. In severe cellulitis, treatment should start with
intravenous cloxacillin (1 g every 6 hours). Intravenous vancomycin (500 mg
every 8 hours if renal function is normal) and teicoplanin (1 g daily) are
alternatives for patients allergic to penicillin. An aminoglycoside may be
added when the clinical setting suggests that gram-negative bacilli may play a
role (e.g., perianal cellulitis, neutropenia, glucocorticoid therapy, and
diabetes mellitus), although monotherapy with second- or third-generation
cephalosporins is an alternative in these situations.
Erysipelas usually responds to intravenous penicillin G (1 million units every
6 hours). Orbital cellulitis is managed with broad-spectrum antibiotics.
Computed tomographic evidence of an abscess or intracranial involvement and
failure to respond to antibiotics within 48 hours are indications for prompt
exploration and decompression of the orbit. Erysipeloid responds to
amoxicillinclavulanate or erythromycin. Animal and human bites necessitate therapy
with oral amoxicilin-clavulanate and local debridement.
While liver function tests are
frequently nonspecific, in certain situations they may be characteristic or
lead one to consider certain groups of disorders. An isolated hyperbilirubinemia
usually suggests a hereditary syndrome. If the elevation is primarily
conjugated, DubinJohnson or Rotor's syndrome come to
mind. If primarily unconjugated, Gilbert's is likely in an adult. However, with
a hemolytic anemia one may also have an unconjugated hyperbilirubinemia. In
Gilbert's the lactate dehydrogenase (LDH) should not be elevated, but in
hemolysis sufficient to cause hyperbilirubinemia the LDH is frequently
In patients with intrahepatic cholestasis or extrahepatic obstruction, there is
a pattern of a significantly elevated alkaline phosphatase and gamma glutamyl
transpeptidase. Patients with primary biliary cirrhosis present initially with
these findings, with bilirubin elevation (usually mild) occurring only late in
the disease. Antimitochondrial antibodies are almost always positive. Though
the total bilirubin rises only slightly most of it is conjugated as reflected
in the direct reacting fraction. Patients with chronic liver disease frequently
have low serum albumin, high serum globulin, and may have elevated prothrombin
times, especially if their liver function is poor.
Alcohol abusers with or without concomitant cocaine abuse and/or trauma may
present with rhabdomyolysis, which may be reflected in an elevated creatine
phosphokinase (CPK), LDH, and possibly AST.
Patients who present with relatively recent onset of jaundice without
antecedent history of liver disease and who deteriorate clinically may be
developing fulminant hepatic failure. Clinically the bilirubin rises, the PT
INR rises markedly, and the patient's mental status
deteriorates. The albumin also tends to become lower and the globulins rise.
Patients with metastatic liver disease generally exhibit an elevated alkaline
phosphatase and a-glutamyl transpeptidase (GGT). This pattern is seen in other
infiltrating diseases as with granulomas in tuberculosis and sarcoidosis and
may be noted in incomplete biliary obstruction.
Patients with cholelithiasis may pass a stone into the common duct, thereby causing
obstruction. When the obstruction is complete, an ascending cholangitis may
present with the classical Charcot's triad of marked jaundice, fever, and right
upper quadrant pain. When the obstruction is relatively acute, the prothrombin
time should be near normal. There may be elevations of the AST and ALT as well
as the prominent elevations of the alkaline phosphatase and GGT, which, as
noted above, are the hallmarks of cholestasis. An elevated alkaline phosphatase
with a normal GGT suggests a cause other than liver disease, such as bone
pathology, pregnancy, or a growing teenager.
Acute viral hepatitis, which is not fulminant, may present with or without
jaundice. Frequently the enzymes are markedly elevated into the thousand range.