Purpura/Petechiae/Excessive Bleeding

Differential Overview

Purpura

❑Trauma

❑Senile purpura

❑Drugs

❑Vasculitis

❑Vitamin K deficiency

❑Psychogenic purpura

❑Cholesterol emboli

❑Warfarin necrosis

❑Scurvy

❑Thrombotic thrombocytopenic purpura

❑Henoch-Schonlein purpura

❑Amyloidosis

Petechiae

❑Autoimmune thrombocytopenia

❑Bacteremia

❑Hypersplenism

Excessive Bleeding

❑Over-anticoagulation

❑Thrombocytopenia

❑von Willebrand disease

❑Circulating anticoagulant

❑Disseminated intravascular coagulation

❑Hemophilia

Diagnostic Approach

A patient with a suspected bleeding disorder should be questioned about response to trauma, past bleeding problems, for example with surgery or dental extractions, history of transfusion, menstrual history and dietary habits. Absence of abnormal bleeding with surgery, significant trauma, or dental extractions makes an inherited bleeding disorder unlikely.

Petechiae are small capillary hemorrhages resulting from platelet or vascular abnormalities. Petechiae on the lower extremities or mucous membranes are usually caused by thrombocytopenia. Tender, elevated petechiae plus abnormalities in other organs suggests vasculitis. Platelet defect disorders produce petechiae and ecchymoses occurring immediately after local trauma. Bleeding is superficial, occurring in the skin, the mucous membranes, the nose, and the gastrointestinal and genitourinary tracts. Bleeding does not occur with normal platelets until the count falls to less than 50,000, and the threshold for important bleeding is 20,000. Oozing blood around catheters suggests DIC, vitamin K deficiency, or platelet abnormalities.

Large-area bruising occurs with vitamin-K–dependent factor deficiency, but not with hemophilia. Plasma protein disorders produce bleeding in deep tissues, such as joints, muscle, and retroperitoneum. The onset of such bleeding can be delayed for hours after trauma.

Palpable purpura is seen with autoimmune or infectious (e.g., meningococcemia, endocarditis) vasculitis. Infectious emboli have an irregular outline, whereas lesions of leukocytoclastic vasculitis are circular.

Clinical Findings

Trauma  Local ecchymoses will be well circumscribed. Patients frequently present with ecchymosis for which they cannot recall trauma.

Senile purpura  Sharply demarcated bruises occur on the extensor forearms in the elderly or patients on steroids. The skin is thinned and moves loosely.

Drugs  Heparin and warfarin have intended anticoagulant effects, but excess may produce widespread ecchymoses in response to trivial trauma. Penicillin, quinidine, quinine, phenytoin, trimethoprim, furosemide, gold salts, carbamazepine, and methyldopa may cause autoimmune thrombocytopenia. Chemotherapeutic agents, thiazides, and estrogens may produce myelosuppression. Aspirin and NSAIDs inhibit platelet aggregation but usually only produce mild clinical bleeding, such as easy bruising or oozing following tooth extractions. Drug hypersensitivity reactions (sulfonamides, penicillin, tetracycline, quinidine, guanethidine, phenothiazines, and propylthiouracil) may produce palpable purpura.

Vasculitis  Recognized as palpable purpura or petechiae that do not blanch, they arise in dependent areas. The skin often burns or itches. Vesicles and necrotic ulcerations may also develop. Precipitants include drug hypersensitivity reactions, connective tissue diseases (rheumatoid arthritis or systemic lupus erythematosus), or infections such as hepatitis C, which causes cryoglobulinemia. There will usually be concomitant signs of systemic vasculitis such as fever or arthralgias.

Vitamin K deficiency  Deficiency is found with inadequate dietary intake, malabsorption, and chronic liver disease. The latter patients are especially predisposed to upper gastrointestinal hemorrhage from varices or alcohol-induced gastritis.

Psychogenic purpura  These patients have spontaneous painful ecchymoses surrounded by erythema and edema as well as other pronounced psychoneurotic complaints.

Cholesterol emboli  A purpuric livedo reticularis, cyanosis, and ultimately ischemic ulcerations occur in the legs and feet of patients with extensive atherosclerosis. The onset often coincides with aortic catheterization.

Warfarin necrosis  A reaction to warfarin may occur, which starts with painful erythema, progresses to purpura, and ultimately develops into necrosis in areas of subcutaneous fat.

Scurvy  Vitamin C deficiency is associated with painful perifollicular hemorrhages with corkscrew hairs, ecchymoses, bleeding into the muscles, and oozing from the gums.

Thrombotic thrombocytopenic purpura  A febrile patient who is in a toxic state presents with abdominal pain and prominent fluctuating neurologic signs.

Henoch-Schonlein purpura  Purpura appears over the lower extremities and buttocks, along with manifestations such as urticaria, edema, fever, headache, anorexia, arthralgias, colicky abdominal pain with melena, and hematuria. It is unusual in adults.

Amyloidosis  Pink, translucent periorbital lesions easily develop purpura when the skin is pinched (“pinch purpura”).

Autoimmune thrombocytopenia  The sudden appearance of crops of hydrostatic petechiae (on the lower extremities) follows a viral exanthem, upper respiratory illness, or mononucleosis-like syndrome. It may also be a presenting finding of HIV infection or lupus. Other associated viruses include HSV, CMV, EBV, VZV, HBV, rubella, mumps, and enteroviruses, recognized by their typical manifestations.

Bacteremia  Endocarditis-associated petechiae appear in the mucous membranes and extremities, including splinter hemorrhages in the nail beds. Gonococcemia lesions on the extremities become pustular, and then hemorrhagic and necrotic. Meningococcemia lesions develop rapidly, are broad and hemorrhagic, and predominate on the trunk. Rocky Mountain Spotted Fever lesions begin as pink macules on the wrists, soles, ankles, and palms, and spread centripetally. By the fourth day, they become petechial and papular, and then hemorrhagic and ulcerated.

Hypersplenism  Thrombocytopenia with splenic enlargement occurs in states of passive congestion (e.g., portal hypertension or congestive heart failure) and with splenic sequestration due to antibody-coated platelets.

Over-anticoagulation  Suspect in a patient on warfarin.

von Willebrand disease  It is an autosomal dominant trait; thus, determining if there is a family history of a bleeding disorder is helpful. Clinical bleeding may occur only after major surgery or trauma, or it may occur spontaneously from the mucosa of the nose, gastrointestinal tract, or genitourinary tract.

Circulating anticoagulant  Common causes of a circulating inhibitor of a procoagulant protein include lupus, the postpartum state, rheumatoid arthritis, AIDS, and penicillin. These produce abnormal coagulation tests and arterial or venous thromboses more often than clinical bleeding.

Disseminated intravascular coagulation  The clinical presentation includes simultaneous bleeding from multiple sites, and livedo reticularis and acrocyanosis due to microthrombi. Purpura fulminans occurring with gram-negative sepsis presents with extensive skin hemorrhage leading to necrosis. DIC occurs most commonly in the setting of obstetrical catastrophe, sepsis, massive trauma, or metastatic cancer. Heat stroke, transfusion reaction, and snakebite can also initiate DIC.

Hemophilia  Family history, recurrent hemarthroses, and excessive bleeding following common hemostatic stresses such as dental extractions, childbirth, or minor surgery are prominent features. Bleeding into joints, muscles, mucous membranes, or the genitourinary tract may occur with trivial injury. Of note, family history may be negative in up to 40% of patients with hemophilia A.

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Book Source Details

• Book Title: Field Guide to Bedside Diagnosis
• Author(s): David S. Smith
• Year of Publication: 2007
• Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2007 Lippincott Williams & Wilkins.

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Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2008 Williams & Wilkins.

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• Back to symptom: Hemorrhagic rash: Introduction (review 7 causes)
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More About This Book: Title: Field Guide to Bedside Diagnosis Authors: David S. Smith Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 0-78178-165-5

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