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Kasabach-Merritt Syndrome

  • Author: Alexandra C Cheerva, MD, MS; Chief Editor: Hassan M Yaish, MD  more...
 
Updated: May 24, 2016
 

Practice Essentials

The combination of giant hemangioma, thrombocytopenia, and consumptive coagulopathy is termed Kasabach-Merritt syndrome (KMS). KMS is an infrequent but potentially fatal complication of rapidly growing vascular lesions in infants. See the image below.

Back of an arm showing the typical bruising associ Back of an arm showing the typical bruising associated with Kasabach-Merritt Syndrome.

Signs and symptoms

Signs and symptoms in KMS include the following:

  • Visible cutaneous giant hemangioma or multiple smaller hemangiomas, usually on the extremities
  • Enlarged abdomen
  • Hepatomegaly or jaundice
  • Petechiae, bruising, and frank bleeding
  • Painful lesions
  • Anemia

Physical findings may include the following:

  • Cutaneous hemangioma, often appearing as a large irregular bruise anywhere on the body and often circumscribed by widespread, overlying, shiny and dusky, purple skin
  • Kaposiform hemangioendothelioma (KHE) or tufted angioma (TA) - Blue or reddish-brown discoloration and skin induration
  • Petechiae and bruising
  • Painful, tender lesions
  • Bleeding from thrombocytopenia and coagulopathy (locally and, at times, distantly [disseminated intravascular coagulation (DIC)])
  • Tachycardia, feeding difficulty, and shock (signs of high-output cardiac failure)
  • Pallor (suggestive of anemia)

See Presentation for more detail.

Diagnosis

Any infant with unexplained thrombocytopenia, with or without evidence of DIC, should be evaluated for visceral or hidden vascular lesions (especially of the liver or spleen).

Laboratory studies that may be helpful include the following:

  • Complete blood count (CBC) count with differential, reticulocyte count, platelet count, and peripheral smear examination
  • Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - These are prolonged in patients with significant DIC
  • Fibrinogen, fibrin degradation product (FDP), and D-dimer levels - The first are reduced in DIC, and the second and third are elevated
  • Blood culture (to exclude sepsis)
  • Chromosome tests (to exclude certain genetic syndromes)

Diagnostic imaging is obtained as appropriate and may include the following:

  • Radiography
  • Computed tomography (CT)
  • Magnetic resonance imaging (MRI)
  • Doppler flow studies

Radionuclide scanning

Although formal staging is not usually performed, documenting the extent of the invasion of the hemangioma into normal tissue is important for possible subsequent treatment with surgery or radiation. Hemangiomas do not metastasize.

See Workup for more detail.

Management

No single pharmacologic therapy has been proved most effective in patients with KMS. Agents that have been tried (most of them not specifically FDA-approved for this application), with varying success, include the following:

  • Corticosteroids (most commonly used)
  • Interferon alfa
  • Aminocaproic acid (to treat bleeding)
  • Aspirin
  • Dipyridamole
  • Ticlopidine
  • Pentoxifylline
  • Cryoprecipitate
  • Heparin
  • Vincristine (80% response reported)
  • Cyclophosphamide
  • Actinomycin D
  • Propranolol (unlike in infantile hemangioma, response is poor)

Nonpharmacologic treatment modalities include the following:

  • Surgical resection (when lesions are not too large or surgically inaccessible) - Wide local excision is recommended but may be difficult; amputation may be necessary for intractable lesions involving a limb
  • Interventional radiologic procedures (when surgical treatment is not feasible)
  • Intermittent pneumatic compression (most useful for a vascular lesion located on an extremity)
  • Radiation therapy (now largely abandoned because of long-term adverse effects)

See Treatment and Medication for more detail.

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Background

The Kasabach-Merritt syndrome (KMS) was first described in 1940 in a male infant with a large, rapidly enlarging discolored lesion on his thigh that was associated with consumptive coagulopathy and thrombocytopenia. The lesion in this original case was a kaposiform hemangioendothelioma, not a classic infantile hemangioma. The combination of enlarging vascular lesion (either a kaposiform hemangioendothelioma or a tufted angioma), profound thrombocytopenia, microangiopathic hemolytic anemia, and consumptive coagulopathy is termed KMS or Kasabach-Merritt phenomenon (KMP).[1, 2]

The vascular lesion may be an obvious superficial lesion or a lesion within a visceral organ or even within the brain. Thrombocytopenia is often severe (ie, platelet count < 50,000/µL). Thrombocytopenia and consumptive coagulopathy are not complications of all vascular lesions, and size alone does not determine which vascular lesions are associated with thrombocytopenia and coagulopathies. KMS is infrequent but has a potentially fatal outcome (reported at 40% in one report) and is characterized by rapid growth of the vascular lesions in infants.[3]  Infantile hemangiomas, the most common tumors of infancy, typically undergo rapid postnatal growth for several months, followed by a prolonged phase of involution.

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Pathophysiology and Etiology

The thrombocytopenia associated with vascular lesions is caused by a localized consumptive coagulopathy. The vascular lesion triggers an intravascular coagulation with platelet trapping, consequent thrombocytopenia, and fibrinogen consumption and degradation, as well as activation and consumption of coagulation factors, resulting in disseminated intravascular coagulation (DIC).[4]  Activation of platelets also promotes further growth of vascular tissue. 

KMS is associated with the two following rare vascular lesions::

  • Kaposiform hemangioendothelioma (KHE) [5]
  • Tufted angioma (TA) [6]

The phenomenon may be associated with trauma in the area of the vascular lesion.

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Epidemiology

United States and international statistics

Hemangiomas are common vascular tumors that occur in as many as 2.5% of neonates in the United States. Most are benign, and 70-80% regress by the age of 7 years. Some hemangiomas are life-threatening; 1 hemangioma in 300 is associated with coagulopathy.[7] Worldwide, reports of KMS are rare.

Age-, sex-, and race-related demographics

KMS typically occurs in early infancy (< 1 year) or childhood, though prenatal cases (diagnosed with the aid of ultrasonography), newborn presentations, and rare cases in older children and adults have been reported. KMS should be included in the differential diagnosis of unexplained chronic thrombocytopenia at any age.

Boys and men are affected slightly more often than girls and women are. In this respect, KMS differs notably from hemangioma of infancy (infantile hemangioma), which affects girls much more often than it does boys. No racial predilection has been identified.

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Prognosis

When KMS is promptly recognized and properly treated, the prognosis is usually excellent because the DIC resolves as the vascular lesion recedes and because KMS does not recur. Therefore, most children do well if they reach age 2 years. When KMS goes untreated, mortality is 10-37%, primarily due to bleeding secondary to the consumptive coagulopathy.[7] Even after failed treatment, however, the hematologic abnormalities may spontaneously resolve over a few months.

Mortality and morbidity are influenced by the anatomic location, depth, and extent of the vascular lesion. Besides bleeding, other conditions associated with morbidity and mortality are as follows:

  • Visceral involvement (particularly in the retroperitoneal area and mediastinum)
  • Profound thrombocytopenia
  • DIC
  • Severe infection
  • Iatrogenic complications (eg, from procedures such as arterial ligation, arterial embolization, or surgical excision)

Hemolytic anemia resulting from physical damage to the red blood cells (RBCs) may be mild, moderate, or severe. The results of the direct antibody test (DAT) or the Coombs test is negative in patients with anemia, and anemia is secondary to microangiopathic destruction of the RBCs,[8]  manifested by the presence of schistocytes on peripheral blood smear examination (a helpful tool in suggesting the presence of viseral hemangiomas).

Heart failure often occurs in affected infants as a result of the large volume of blood flowing through the giant hemangioma.[9]

An association of KMS with trisomy 21 mosaicism is uncommon; however, 43% of children with Down syndrome have cutaneous vascular lesions. One child with Down syndrome and KMS has been reported.[10]

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Contributor Information and Disclosures
Author

Alexandra C Cheerva, MD, MS Associate Professor of Pediatrics, University of Louisville School of Medicine; Director of Pediatric Blood and Marrow Transplantation, Section of Pediatric Hematology and Oncology, Kosair Children's Hospital

Alexandra C Cheerva, MD, MS is a member of the following medical societies: American Society for Blood and Marrow Transplantation, Children's Oncology Group, American Society of Clinical Oncology, International Pediatric Transplant Association, American Society of Pediatric Hematology/Oncology, Kentucky Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Ashok B Raj, MD Professor, Section of Pediatric Hematology and Oncology, Department of Pediatrics, Kosair Children's Hospital, University of Louisville School of Medicine

Ashok B Raj, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Pediatric Hematology/Oncology, Kentucky Medical Association, Children's Oncology Group

Disclosure: Nothing to disclose.

Salvatore Bertolone, MD Director, Division of Pediatric Hematology/Oncology, Kosair Children's Hospital; Professor, Department of Pediatrics, University of Louisville School of Medicine

Salvatore Bertolone, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for Cancer Education, American Association of Blood Banks, American Cancer Society, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Kentucky Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Hassan M Yaish, MD Medical Director, Intermountain Hemophilia and Thrombophilia Treatment Center; Professor of Pediatrics, University of Utah School of Medicine; Director of Hematology, Pediatric Hematologist/Oncologist, Department of Pediatrics, Primary Children's Medical Center

Hassan M Yaish, MD is a member of the following medical societies: American Academy of Pediatrics, New York Academy of Sciences, American Medical Association, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Michigan State Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

Emmanuel C Besa, MD Professor, Department of Medicine, Division of Hematologic Malignancies and Hematopoietic Stem Cell Transplantation, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Clinical Oncology, American Society of Hematology, and New York Academy of Sciences

Disclosure: Nothing to disclose.

Gary D Crouch, MD Associate Professor, Program Director of Pediatric Hematology-Oncology Fellowship, Department of Pediatrics, Uniformed Services University of the Health Sciences

Gary D Crouch, MD is a member of the following medical societies: American Academy of Pediatrics and American Society of Hematology

Disclosure: Nothing to disclose. Guy B Faguet, MD Former Professor, Department of Medicine, Section of Hematology and Oncology, Medical College of Georgia

Guy B Faguet, MD is a member of the following medical societies: American Association of Immunologists, American Society of Hematology, International Society of Hematology, New York Academy of Sciences, Southern Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Linda K Hendricks, MD Assistant Professor, Department of Internal Medicine, Section of Hematology and Oncology, Mercer University School of Medicine

Linda K Hendricks, MD is a member of the following medical societies: American Society of Hematology

Disclosure: Nothing to disclose.

Gary R Jones, MD Associate Medical Director, Clinical Development, Berlex Laboratories

Gary R Jones, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Pediatric Hematology/Oncology, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Michael Paul Kosty, MD Associate Director, Associate Professor, Department of Internal Medicine, Divisions of Supportive Care Services and Hematology and Oncology, Ida M and Cecil H Green Cancer Center, Scripps Clinic

Michael Paul Kosty, MD is a member of the following medical societies: American College of Physicians, American Society of Hematology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Bernice R Krafchik, MBChB, FRCPC Professor Emeritus, Department of Pediatrics, Section of Dermatology, University of Toronto

Bernice R Krafchik, MBChB, FRCPC is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Dermatology

Disclosure: Nothing to disclose.

Sejal Kuthiala, MD Staff Physician, Department of Internal Medicine, Medical College of Georgia

Sejal Kuthiala, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Ronald A Sacher, MB, BCh, MD, FRCPC Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Clinical and Climatological Association, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society of Blood Transfusion, International Society on Thrombosis and Haemostasis, and Royal College of Physicians and Surgeons of Canada

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

Carlos Suarez, MD Associate Professor, Department of Pediatrics, Section of Pediatric Hematology and Oncology, University of Louisville School of Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Leg with a Kaposiform hemangioendothelioma, lesion associated with Kasabach-Merritt Syndrome.
Back of an arm showing the typical bruising associated with Kasabach-Merritt Syndrome.
 
 
 
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