Scrigroup - Documente si articole


HomeDocumenteUploadResurseAlte limbi doc
BulgaraCeha slovacaCroataEnglezaEstonaFinlandezaFranceza




+ Font mai mare | - Font mai mic



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.

liver function tests

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 abnormal.
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.

Politica de confidentialitate | Termeni si conditii de utilizare



Vizualizari: 1289
Importanta: rank

Comenteaza documentul:

Te rugam sa te autentifici sau sa iti faci cont pentru a putea comenta

Creaza cont nou

Termeni si conditii de utilizare | Contact
© SCRIGROUP 2024 . All rights reserved