China
Africa
Explore chapters and articles related to this topic
Paediatrics
Published in Adnan Darr, Karan Jolly, Jameel Muzaffar, ENT Vivas, 2023
Paula Coyle, Eishaan Bhargava, Adnan Darr, Karan Jolly, Kate Stephenson, Michael Kuo
Investigations: FBC: Platelet consumption (Kasabach-Merritt syndrome) Thrombocytopaenia associated with haemangiotheliomaCaused by platelet trapping within tumourUSS/Doppler to quantify if low or high flowCV examination, ECG, Echo prior to initiation of propranolol (rule out high output CCF)MRI head to rule out posterior fossa lesions (PHACES) or if lesions in upper half of faceMLB for suspected cases
Salivary Glands
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Neil Bateman, Rachael Lawrence
Almost all haemangiomas will involute and surgery should be confined to management of bleeding or ulceration, or to cases where the diagnosis is in doubt.30 Kasabach-Merritt syndrome, a consumptive coagulopathy, is another indication for active intervention.
Practice Paper 1: Answers
Published in Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar, Get ahead! Medicine, 2016
Anthony B. Starr, Hiruni Jayasena, David Capewell
A cavernous haemangioma (or strawberry naevus) is a condition that appears in the first months of life as a bright-red lesion on the face or trunk that grows rapidly. Occasionally, these lesions bleed or ulcerate. Cavernous haemangiomas eventually regress and disappear spontaneously, so intervention is required only if lesions persist beyond a few years of age. Cavernous haemangiomas may rarely be associated with thrombocytopenia and haemolytic anaemia secondary to trapping and destruction of platelets and erythrocytes within the lesions. This is known as Kasabach–Merritt syndrome.
Effectiveness of microwave ablation for the treatment of hepatic hemangioma - meta-analysis and meta-regression
Published in International Journal of Hyperthermia, 2023
Hepatic hemangioma is the most common benign tumor of the liver with small capillary hemangiomata of no clinical significance. Larger cavernous hemangiomata more often come to the attention of the liver surgeon [1]. Usually, patients present with asymptomatic and are diagnosed incidentally on imaging studies. Yet, when the masses keep growing, vague upper abdominal symptoms may manifest. Rapid enlargement or vessel thrombosis of the tumor can occasionally cause symptoms, and spontaneous rupture is exceedingly rare. The associated Kasabach–Merritt syndrome, however rare, is well defined. The prognosis of hepatic hemangioma is generally benign. In most cases, the lesions remain stable over long periods of time, and the constant rupture or large hemorrhage is seldom confronted in clinical practice. No malignant transformation of liver hemangioma has been reported before. Therefore, asymptomatic patients with definitive diagnosis can simply be observed, and symptomatic patients excluding the others causes should be candidates for treatment.
Efficacy of transcatheter arterial chemoembolization combined with sirolimus for treating Kasabach–Merritt phenomenon in infants, a retrospective study
Published in Annals of Medicine, 2023
Chuan-gao Yin, Wei-Wei Qi, Song Wang, Deng Pan, Xiao-Li Chen, Shi-Yu Li
Kasabach–Merritt syndrome (KMS), which refers to giant haemangioma combined with thrombocytopenia syndrome, was first reported by Kasabach and Merritt in 1940 [1]. In the 1990s, it was found that this disease was caused by Kaposiform hemangioendothelioma (KHE) and tufted haemangioma (TA) rather than infantile haemangioma. In the same year, Professor Sarker suggested that severe thrombocytopenia, microangiopathic haemolytic anaemia, secondary fibrinogenopenia, and consumptive coagulation disorder caused by KHE and TA should be known as the Kasabach–Merritt phenomenon (KMP). Infants and young children are prone to KMP. Although the condition is rare, the fatality rate is as high as 10%–37% [2], and there is no agreed treatment regimen. Traditional treatment methods include compression, support, drug therapy, radiotherapy, endovascular embolization, and surgery. Drug therapy includes treatment with prednisone, interferon, propranolol, and sirolimus, added in recent years. However, compression and drug therapies are slow to work. For large lesions, it is usually difficult to surgically resect them completely, and the risk is high. The action time of endovascular embolization alone on platelet elevation is usually limited.