Thrombocytopenia-Absent Radius Syndrome

Updated: Mar 07, 2019
Author: John K Wu, MBBS, MSc, FRCPC; Chief Editor: Hassan M Yaish, MD 



Thrombocytopenia-absent radius (TAR) syndrome is a rare condition in which thrombocytopenia is associated with bilateral radial aplasia. TAR syndrome was first described in 1951. An autosomal recessive inheritance pattern was proposed because TAR affected more than one member of some families. In 1969, TAR was defined as a syndrome and further classified as the association of hypomegakaryocytic thrombocytopenia and absent radii. The expression varies and includes abnormalities in the GI, skeletal, hematologic, and cardiac systems.[1, 2, 3] See the images below.

Infant with thrombocytopenia-absent radius syndrom Infant with thrombocytopenia-absent radius syndrome. The arms and forearms are shortened, with radial deviation of both hands because of the absence of bilateral radii. The legs are normal. See also Media files 2 and 3.
Same infant as in Media files 1 and 3. Close-up ph Same infant as in Media files 1 and 3. Close-up photograph of arm and forearm (volar aspect). Note the petechiae.
Same infant as in Media files 1 and 2. Close-up ph Same infant as in Media files 1 and 2. Close-up photograph of arm and forearm (dorsal aspect).


Some have proposed that the association of seemingly disparate skeletal and hematologic abnormalities is related to the simultaneous development of the heart, the radii, and the megakaryocytes at 6-8 weeks' gestation. The similarity of TAR syndrome to congenital rubella suggests intrauterine injury when the involved systems develop, but a common etiologic agent has not been identified. 

The exact pathophysiology of the thrombocytopenia is still unclear. The platelet abnormality reflects platelet hypoproduction, for which numerous explanatory theories have been proposed. One suggestion is that a failure in production of humoral or cellular stimulators of megakaryocytopoiesis (eg, thrombopoietin) is responsible for inhibiting platelet production. However, studies by Ballmaier and colleagues and Sekine and associates showed comparable or increased levels of thrombopoietin in patients with TAR compared with healthy control subjects.[4, 5] These findings suggest that the thrombocytopenia is due to a lack of response to thrombopoietin, especially given the observation of normal thrombopoietin receptor expression on megakaryocytes; this raises the question of a defect in c-Mpl signaling.

Many mutations have been postulated; however, despite investigations of the c-mpl gene in patients with TAR, no mutations have been found in this gene.[6] Another proposed candidate gene is a HOX gene. The HOX family of genes plays a major role in embryogenesis and cell differentiation, including differentiation of hematopoietic cell lines. However, Fleischman and colleagues did not detect mutations in the coding sequence of HOX genes known to affect radial development.[7]  Subsequently, an interstitial microdeletion of chromosome 1q was identified in 30 patients with TAR syndrome.[8] All patients and 75% of unaffected parents in this cohort had the microdeletion, suggesting co-inheritance of an additional modifier gene for disease expression.

Albers and colleagues applied high-throughput sequencing in 5 unrelated patients with TAR syndrome and the chromosome 1q21.1 deletion.[9] They discovered one low frequency single nucleotide polymorphism (SNP) in the noncoding 5' untranslated (UTR) region of the gene RBM8A in 4 of the cases and another low frequency noncoding SNP in the first intron of the same gene. These findings were further confirmed in 48 individuals with TAR syndrome. The investigators found coinheritance of the 1q21.1 deletion with either SNP, causing significant decreases in the level of Y14, a protein encoded by RBM8A.[10] The exact mechanism for which decreased levels of Y14 produces the phenotype associated with TAR syndrome remains to be elucidated. Y14 is part of the exon-junction complex (EJC), a set of proteins associated with transcript export, localization, and splicing, playing a critical in embryonic development.[11, 12] Some studies have suggested defects in signal transduction downstream of thrombopoietin.

A study by Manukjan et al indicated that in patients with TAR syndrome, those with the 5’UTR SNP in RBM8A have a significantly lower platelet count than do patients with the intron-1 SNP in this gene.[13]

TAR syndrome was initially considered an autosomal recessive disease. Some have suggested that the inheritance pattern may be autosomal dominant with variable penetrance. 



United States

TAR syndrome rarely occurs in the United States.


The frequency of TAR syndrome is 0.42 case per 100,000 live births in Spain.


The major cause of mortality in TAR syndrome is hemorrhage. The incidence of hemorrhage is limited to the first 14 months of life. In a study by Hedberg and associates, 18 of 20 deaths in 76 patients were due to hemorrhagic events; most of patients who died had platelet counts < 10 X 109/L.[14]

Bleeding and hemorrhage can also result in clinically significant morbidity, especially intracranial hemorrhage. Hand and upper-extremity function is usually good if radial aplasia is the only skeletal abnormality. However, patients require plastic surgery, occupational therapy, and physiotherapy.


No ethnic or racial predilection is reported.


The male-to-female ratio is 1:1. Greenhalgh and associates reported an excess of females (27:7),[15] as did Hall and colleagues (26:14).[16]


TAR syndrome is congenital, and patients usually present with symptomatic thrombocytopenia in the first week of life.


The prognosis in TAR is better than in congenital amegakaryocytic thrombocytopenia (CAMT). Survival in TAR plateaus at greater than 70% after age 4 years. The platelet count improves after age 1 year (unlike in CAMT), so platelet transfusion is rarely needed after that.




Episodes of thrombocytopenia begin in the neonatal period in patients with thrombocytopenia-absent radius (TAR) syndrome.[17]

About 50% of affected infants are symptomatic in the first week of life, and 90% are symptomatic by the age of 4 months. Thrombocytopenia can fluctuate over time. Therefore, if TAR syndrome is strongly suspected on the basis of one normal platelet count, repeating the blood work is recommended.

Thrombocytopenic episodes are most frequent during the first 2 years of life, when they increase the mortality rate secondary to intracranial hemorrhage. With increasing age, the recurrence of thrombocytopenic episodes decreases. Thrombocytopenia can improve to a near-normal state.

Nonspecific stress, infection, and diet (eg, allergy to cow's milk) may precipitate episodes. Symptoms include purpura, petechiae, epistaxis, melena, hemoptysis, hematuria, hematemesis, and, rarely, intracranial hemorrhage.

Symptomatic cow's-milk allergy is associated with 47% of all cases of TAR syndrome, and patients may present as vomiting, bloody diarrhea, and failure to thrive.

Mental retardation is associated with about 7% of all cases of TAR syndrome. The association of TAR with mental retardation is presumed to be secondary to complications from intracranial hemorrhage precipitated by thrombocytopenia.

Symptoms of acute intracranial hemorrhage in an infant are associated with poor feeding, lethargy, irritability, and fluctuating levels of consciousness.

Structural causes that predispose the patient to mental retardation and other neuropsychiatric disorders (psychosis) have been suggested.[18]

Hypoplasia of the cerebellar vermis and corpus callosum has been reported in this syndrome.[19]


Upper-extremity abnormalities range from isolated absent radii to phocomelia. Abnormalities include the following:

  • Bilateral radial aplasia

  • Radial club hand

  • Hypoplastic carpals and phalanges

  • Hypoplastic ulnae, humeri, and shoulder girdles

  • Syndactyly and clinodactyly of fingers and toes

  • Selective hypoplasia of middle phalanx, fifth digit

  • Altered palmar contours

Greenhalgh and colleagues examined 34 patients with TAR syndrome.[15] Their findings demonstrated how the length of the upper limb can affect the patient's functional ability. They divided upper-limb defects into 3 categories of severity, as follows:

  • The first group (71%) had mild defects consisting of radial aplasia with various degrees of ulnar and humeral hypoplasia. The patients also had normal shoulder girth and, hence, near-normal upper-body strength, but splints were still useful for periods of prolonged activity of the upper limbs.

  • The second group (18%) had increased degrees of limb shortening, humeral hypoplasia, and underdevelopment of the shoulder girth with decreased upper-body strength. Splints were also useful in this group.

  • The last group was the most affected, with severe ulnar and humeral shortening and phocomelia.

Lower-extremity anomalies occur in 46% of patients and vary from clinically undetectable changes to phocomelia. These anomalies are usually less severe than those of the upper limbs. Abnormalities include the following:

  • Hip dislocation

  • Femoral torsion

  • Tibial torsion

  • Valgus and varus foot deformities

  • Deformity of the knee (eg, absence of the patella, patellar dislocation)

  • Absent tibiofibular joint

  • Abnormal toe placement

  • Fifth toe overlapping the fourth

Cardiac anomalies occur in 15-33% of patients and include the following:

  • Tetralogy of Fallot

  • Atrial septal defect

  • Ventricular septal defect (VSD)

Facial anomalies (which occur in 53% of patients) include the following:

  • Micrognathia (3-30% of patients)

  • Tall, broad forehead

  • Facial hemangiomas

  • Hypertelorism

  • Low, posteriorly rotated ears

Other abnormalities are numerous and include the following:

  • Asymmetric first rib

  • Cervical rib, cervical spina bifida, fused cervical spine, and nuchal folds

  • Meckel diverticulum

  • Uterine anomalies

  • Dorsal pedal edema

  • Hyperhidrosis

  • Short stature (95% of patients at or below the 50th percentile)

  • Other skeletal malformations

  • Renal anomalies (23% of patients), eg, duplex ureter, mild renal pelvis dilatation, horseshoe kidneys

  • Intracranial vascular malformation

  • Sensorineural hearing loss

  • Cleft palate

  • Scoliosis

  • GI anomalies (eg, esophageal atresia, tracheoesophageal fistula, anal atresia)

  • Annular pancreas

Only patients with TAR syndrome consistently have bilateral absence of the radii with the presence of thumbs and 4 digits. In distinguishing TAR from other syndromes involving skeletal abnormalities of the upper extremities, the following features may be of assistance:

  • Patients with TAR syndrome always have thumbs, but thumbs are usually absent or hypoplastic in patients with Fanconi anemia and radial defects. Fanconi anemia is also associated with chromosomal fragility, a rare onset of thrombocytopenia before age 1 year, and pancytopenia in children aged 5-10 years. A reliable diagnostic test is a chromosomal breakage study.

  • Thumb abnormalities include absent, hypoplastic, and triphalangeal thumbs in Holt-Oram syndrome, and blood counts are normal. The patient often has a family history of heart and limb defects due to the autosomal dominant pattern of inheritance.

  • Thrombocytopenia is not often observed in Roberts syndrome (Roberts-SC phocomelia). Most patients with this syndrome have microcephaly and mental retardation.

  • Radial hypoplasia is found in patients with Aase syndrome, but the thumb is triphalangeal. Hypoplastic anemia is the usual presentation, similar to that of Blackfan-Diamond syndrome. Thrombocytopenia is not a feature.


Causes of TAR syndrome are not fully elucidated. See Pathophysiology.



Diagnostic Considerations

Fanconi anemia

The manifestations of TAR and Fanconi anemia frequently overlap. The following features may help to differentiate the two conditions:

  • In Fanconi anemia, thrombocytopenia is rarely present at birth; it develops later on in childhood or even in adulthood
  • Radial defects are seen in only 30% of patients with Fanconi anemia; when present, such defects are usually associated with absent thumb, unlike in TAR, where radial defects are the sine qua non and the thumb is usually present, even though it could be abnormal
  • Chromosome fragility is a diagnostic feature of Fanconi anemia; TAR patients should probably be tested for this to exclude Fanconi anemia


Amegakaryocytic thrombocytopenia with radioulnar synostosis (ARTUS) is usually associated with a HOXA11 gene mutation, a condition of autosomal dominant inheritance.[20, 21] The thrombocytopenia persists and does not improve with age. Furthermore, aplastic anemia may develop later in life.


RAPADILINO syndrome is a rare syndrome characterized by radial hypoplasia or aplasia, patellar hypoplasia or aplasia, cleft or highly arched palate, diarrhea, dislocated joints, small size (>2 standard deviations below the mean in height), limb malformation, slender nose, and normal intelligence.

Roberts syndrome

Roberts syndrome is characterized by prenatal and postnatal growth retardation; craniofacial anomalies, especially facial clefts; limb deficiencies, including tetraphocomelia in most patients; and genital hyperplasia. Parental consanguinity rate is high.

Thalidomide embryopathy

Thalidomide embryopathy is the teratogenic effect of thalidomide when the drug is taken during pregnancy. Affected infants can have limb and digit defects, craniofacial anomalies, hearing and vision defects, and improper formation of organs including the heart and kidneys.

Trisomy 18 (Edward syndrome)

Patients with trisomy 18 may have craniofacial anomalies (eg, prominent occiput, short palpebral fissures, micrognathia, external ear variations); digit anomalies (eg, clenched fist with the index finger overlapping the third finger, the fifth finger overlapping the fourth, hypoplastic nails, thumb aplasia); short sternum (breastbone); rocker-bottom feet; and cardiac, pulmonary, GI, and genitourinary defects.This conditon is frequently associated with thrombocytopenia. However patients also exhibit esophageal dysplasia.

VACTERL association

This is a syndrome of congenital anomalies that includes vertebral dysgenesis, anal atresia with or without fistula, cardiac defects (ventricular septal defect [VSD]), tracheoesophageal fistula, and renal and limb anomalies.

Differential Diagnoses



Laboratory Studies

CBC count

The platelet count is frequently less than 50 X 109/L ( 15-30 X 109/L.) Platelet morphology looks normal on blood smear examination. Large platelets are not a feature.  Eosinophilia is observed in 50% of patients.

Leukocytosis may be present, with a WBC count >35 X 109/L with a left shift and picture of leukemoid reaction.

Anemia may be present secondary to bleeding.

Genetic findings

Chromosomes are normal. Findings on chromosomal breakage studies with clastogenic agents are normal.

Imaging Studies

Characteristic skeletal involvement (ie, absent radii) is detectable during prenatal transvaginal ultrasonography as early as 13 weeks' gestation, when sufficient fetal skeletal ossification is present.

Upper-limb abnormalities on prenatal sonograms suggest numerous syndromes in the differential diagnosis.

After radial aplasia is observed, ultrasonography of the extremities, face, and kidneys is indicated.

Other Tests

Sampling of the bone marrow (which is not required to make the diagnosis) reveals the following findings:

  • Normal or hypercellular bone marrow

  • Decreased, absent, or immature megakaryocytes

  • Small, basophilic, vacuolated megakaryocytes

  • Erythroid hyperplasia


Cordocentesis can be performed to confirm known genetic conditions. Cordocentesis poses a 1-2% risk of fetal loss and a risk of prolonged bleeding from the umbilical puncture site.

Weinblatt and associates performed in utero platelet transfusion of a fetus with radial aplasia at 37 weeks' gestation after cordocentesis revealed a platelet count of 40 X 109/L.[22] The infant was delivered within 24 hours of the transfusion with no complications.



Medical Care

In patients with thrombocytopenia-absent radius (TAR) syndrome, general thrombocytopenic precautions during times of clinically significant thrombocytopenia with a platelet count < 80 X 109/L (usually during the first year of life) should include avoidance of trauma (with use of a soft helmet if needed), avoidance of certain antiplatelet drugs (eg, aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs]), and prolonged pressure on injection sites (especially after intramuscular injections).[23]

Prehospital care should involve first aid for visible acute hemorrhage. Apply firm steady pressure to the site of bleeding. Keep the patient warm. Elevate the bleeding limb.

The mainstay of hospital treatment is supportive care. By far, the most important treatment is platelet transfusion. The goal of platelet transfusion is to maintain a sufficient volume of platelet to prevent bleeding without adverse effects.

Prophylactic transfusions with leukocyte-reduced platelet concentrates are used in patients at high risk of clinically significant hemorrhage.

A transfusion target extrapolated from thrombocytopenia associated with acute leukemia is a platelet count < 40 X 109/L. Platelet counts greater than this level are associated with a decreased risk of major vascular bleeding. Melena, epistaxis, hematuria, mucosal bleeding, and hematemesis are controlled in 80% of patients with acute leukemia when a posttransfusion increment of >40 X 109/L is used.

Potential risks of platelet transfusion include infection, anaphylaxis, formation of antiplatelet antibodies, and hemolytic reactions.

Hepatitis viruses (B, C, other) and HIV are the most common infective pathogens potentially transmitted with the transfusion of blood products.

A further risk with transfusion is human leukocyte antigen (HLA) alloimmunization. However, platelets themselves are not highly immunogenic, and contaminating lymphocytes are most likely to cause HLA alloimmunization. Therefore, leukocyte-reduced platelet concentrates should always be used. Alloimmunization can be delayed by using random single-donor platelets and, ideally, by identifying a limited number of dedicated donors.

Treatment of conditions refractory or nonresponsive to transfusion is difficult but may include the use of HLA-matched platelets from family members. However, the refractory state can occur even in patients receiving HLA-matched platelets, a finding that suggests a non-HLA, platelet-specific antigen.

Splenectomy may be partially effective for the treatment of thrombocytopenia in adults.

Hematopoietic stem cell transplantation (HSCT) is an option for patients who remain thrombocytopenic with bleeding despite platelet transfusions.

Patients with thrombocytopenia have responded to cytokine treatment with erythropoietin and interleukin-6. The side effects of the latter, however, do not justify such therapy.[24, 25]

Surgical Care

Splinting of the hands (and legs, if indicated) during infancy improves future function. If surgical correction of the arm deformities is indicated, it should be undertaken after the patient is hemodynamically stable. If surgery is not a feasible option to manage deformities of the upper limb as patients age, adaptive devices to assist with activities of daily living (eg, dressing, toileting, feeding) are helpful. Prostheses are less useful than adaptive devices because the patient often has a weak upper extremity because of poorly developed musculature and because a functional 5-digit hand diminishes the need for a long limb.

Management of lower-extremity deformities must be individualized given the wide spectrum of anomalies. Intervention can range from no treatment if the deformity is mild (eg, mild varus deformity) and if it causes no functional impairment to the use of a power wheelchair or a motorized cart if the anomaly is severe and if it limits ambulation. Overall, the goal is to improve functioning and enhance independence.

Splenectomy may be partially effective for the treatment of thrombocytopenia in adults.


The patient with suspected TAR syndrome should be examined by a hematologist, orthopedic surgeon, plastic surgeon, and cardiologist, all of whom specialize in treating children.


Patients should avoid ingesting cow's milk for the first year of life because cow's milk allergy is associated with TAR and may precipitate thrombocytopenic episodes.

The frequency of thrombocytopenic episodes and the risk of complications are typically highest during the first 2 years of life, and recurrences decrease as the child ages.

Bloody diarrhea is reported in 20% of patients. Removal of milk from the diet alleviates this symptom.


Careful handling of the patient, with padding of his or her crib and with the application of soft helmets, can be used in the first year of life. Most patients are adequately hemostatic after the first year of life to allow them to perform normal activities. Patients should avoid trauma (eg, contact sports) during periods of thrombocytopenia.

A study by Al Kaissi et al indicated that optimal treatment of TAR syndrome can allow patients to participate in most activities of daily living, albeit with some ulnar deviation and with limitations on wrist extension and on total active range of digital motion. The study included five patients, in whom the wrists underwent realignment and stabilization and whose ulnar forearm bows were reversed through rebalancing of the musculotendinous forces around the wrist.[26]



Medication Summary

The use of antifibrinolytic agents and synthetic antidiuretic hormones may be indicated.

Antifibrinolytic agents

Class Summary

Antifibrinolytic agents decrease bleeding and transfusion requirements and help establish hemostasis. They are especially useful for controlling bleeding or prolonged oozing from gingival surfaces (eg, during teething in infants).

Aminocaproic acid (Amicar)

Competitively inhibits activation of plasminogen to plasmin.

Tranexamic acid (Cyklokapron)

Competitively inhibits activation of plasminogen to plasmin.

Synthetic antidiuretic hormones

Class Summary

Synthetic antidiuretic hormones nonspecifically enhance hemostasis by stimulating the release of von Willebrand factor. Desmopressin stimulates the release of factor VIII, prostaglandins, and plasminogen. However, the mechanism of action is not clear, and it may not be common to all 3 substances. These agents affect vascular walls, increasing platelet adhesion. This local hemostatic action may account for their hemostatic properties.

Desmopressin acetate (DDAVP)

Increases plasma factor VIII levels, promoting platelet aggregation. Intranasal route not recommended because of unproven efficacy in small infants. Only concentrated form (150 mcg/spray) enhances hemostasis.



Further Outpatient Care

Monitor the need for and response to platelet transfusions by measuring platelet counts.

Further Inpatient Care

Monitor response to platelet transfusions through observation of hemostasis and rise in platelet counts in patients with thrombocytopenia-absent radius (TAR) syndrome.


Although the patient is thrombocytopenic, injury-prevention strategies are indicated.

Patients should avoid contact sports and use appropriate protective gear (eg, helmets, padding) when participating in sports or leisure activities.


Complications arise from hemorrhage and hemorrhagic insults, especially intracranial hemorrhage.


The clinical course is one of episodic, severe thrombocytopenia superimposed on a background of persistent thrombocytopenia. The frequency of thrombocytopenic episodes decreases with age. By school age, near-normal platelet counts are expected. If a patient survives the initial 2 years of life, life expectancy is normal.

The risk of morbidity may be increased. Case reports describe acute leukemia in both pediatric and adult patients with TAR syndrome. This development is not entirely unexpected because other syndromes of bone marrow failure, such as Fanconi anemia and Shwachman-Diamond syndrome, are associated with an increased risk of malignancies. Given the rare incidence of this syndrome, however, identifying a chance association or a causal relationship is difficult.

Jameson-Lee et al reported on an adult male patient with TAR syndrome in whom myelodysplastic syndrome progressed to acute myeloid leukemia (AML). The patient also had a CALR driver mutation, which is uncharacteristic of individuals with TAR syndrome, and no RBM8A mutation, despite the association of this mutation with the syndrome. A review of the literature turned up three other TAR syndrome patients with AML, only one of whom was an adult, and one patient in whom acute lymphoblastic leukemia developed.[27]

Patient Education

Patients and families must be educated about the risk of hemorrhagic injury during episodes of thrombocytopenia, about signs and symptoms indicative of thrombocytopenia (eg, bruising, petechiae, mucosal bleeding), and about the need to promptly seek medical attention during these episodes.

For excellent patient education resources, see eMedicineHealth's patient education article Bone Marrow Biopsy.


Questions & Answers


What is thrombocytopenia-absent radius (TAR) syndrome?

What is the pathophysiology of thrombocytopenia-absent radius (TAR) syndrome?

What is the prevalence of thrombocytopenia-absent radius (TAR) syndrome in the US?

What is the global prevalence of thrombocytopenia-absent radius (TAR) syndrome?

What is the mortality and morbidity associated with thrombocytopenia-absent radius (TAR) syndrome?

What are the racial predilections of thrombocytopenia-absent radius (TAR) syndrome?

What are the sexual predilections of thrombocytopenia-absent radius (TAR) syndrome?

At what age is thrombocytopenia-absent radius (TAR) syndrome typically diagnosed?

What is the prognosis of thrombocytopenia-absent radius (TAR) syndrome?


Which clinical history findings are characteristic of thrombocytopenia-absent radius (TAR) syndrome?

Which upper-extremity findings are characteristic of thrombocytopenia-absent radius (TAR) syndrome?

How is the severity of thrombocytopenia-absent radius (TAR) syndrome categorized?

Which lower-extremity findings are characteristic of thrombocytopenia-absent radius (TAR) syndrome?

Which cardiac findings are characteristic of thrombocytopenia-absent radius (TAR) syndrome?

Which facial anomalies are characteristic of thrombocytopenia-absent radius (TAR) syndrome?

Which physical findings are characteristic of thrombocytopenia-absent radius (TAR) syndrome?

How is thrombocytopenia-absent radius (TAR) syndrome differentiated from other skeletal conditions of the upper extremities?


How is thrombocytopenia-absent radius (TAR) syndrome differentiated from Fanconi anemia?

How is thrombocytopenia-absent radius (TAR) syndrome differentiated from amegakaryocytic thrombocytopenia with radioulnar synostosis (ARTUS)?

How is thrombocytopenia-absent radius (TAR) syndrome differentiated from RAPADILINO syndrome?

How is thrombocytopenia-absent radius (TAR) syndrome differentiated from Roberts syndrome?

How is thrombocytopenia-absent radius (TAR) syndrome differentiated from thalidomide embryopathy?

How is thrombocytopenia-absent radius (TAR) syndrome differentiated from trisomy 18 (Edward syndrome)?

How is thrombocytopenia-absent radius (TAR) syndrome differentiated from VACTERL (vertebral defects, anal atresia, cardiac defects, tracheoesophageal fistula, renal anomalies, and limb abnormalities)?

What are the differential diagnoses for Thrombocytopenia-Absent Radius Syndrome?


What is the role of CBC count in the diagnosis of thrombocytopenia-absent radius (TAR) syndrome?

Which genetic findings are characteristic of thrombocytopenia-absent radius (TAR) syndrome?

What is the role of imaging studies in the workup of thrombocytopenia-absent radius (TAR) syndrome?

Which bone marrow findings are characteristic of thrombocytopenia-absent radius (TAR) syndrome?

What is the role of cordocentesis in the workup of thrombocytopenia-absent radius (TAR) syndrome?


How is thrombocytopenia-absent radius (TAR) syndrome treated?

What is the role of surgery in the treatment of thrombocytopenia-absent radius (TAR) syndrome?

Which specialist consultations are beneficial to patients with thrombocytopenia-absent radius (TAR) syndrome?

Which dietary modifications are used in the treatment of thrombocytopenia-absent radius (TAR) syndrome?

Which activity modifications are used in the treatment of thrombocytopenia-absent radius (TAR) syndrome?


What is the role of medications in the treatment of thrombocytopenia-absent radius (TAR) syndrome?

Which medications in the drug class Synthetic antidiuretic hormones are used in the treatment of Thrombocytopenia-Absent Radius Syndrome?

Which medications in the drug class Antifibrinolytic agents are used in the treatment of Thrombocytopenia-Absent Radius Syndrome?


How is response to platelet transfusion monitored in thrombocytopenia-absent radius (TAR) syndrome treatment?

What is included in inpatient care for thrombocytopenia-absent radius (TAR) syndrome?

How are injuries prevented in patients with thrombocytopenia-absent radius (TAR) syndrome?

What are the possible complications of thrombocytopenia-absent radius (TAR) syndrome?

What is the prognosis of thrombocytopenia-absent radius (TAR) syndrome?

What is included in patient education about thrombocytopenia-absent radius (TAR) syndrome?