Thrombocytopenia is common among sick neonates, affecting 20–35% of all patients admitted to the neonatal intensive care unit (NICU). While most cases of neonatal thrombocytopenia are mild or moderate and resolve within 7–14 days with appropriate therapy, 2.5–5% of NICU patients develop severe thrombocytopenia, sometimes lasting for several weeks and requiring >20 platelet transfusions. The availability of thrombopoietic agents offers the possibility of decreasing the number of platelet transfusions and potentially improving the outcomes of these infants. Adding thrombopoietin (TPO) mimetics to the therapeutic armamentarium of neonatologists, however, will require careful attention to the substantial developmental differences between neonates and adults in the process of megakaryocytopoiesis and in their responses to TPO. Taken together, the available data suggest that TPO mimetics will stimulate platelet production in neonates, but might do so through different mechanisms and at different doses than those established for adults. In addition, the specific groups of thrombocytopenic neonates most likely to benefit from therapy with TPO mimetics need to be defined, and the potential non-hematological effects of these agents on the developing organism need to be considered. This review summarizes our current understanding of neonatal megakaryocytopoiesis, and examines in detail the developmental factors relevant to the potential use of TPO mimetics in neonates.
Thrombocytopenia affects up to 35% of all patients admitted to the neonatal intensive care unit (NICU). The causes of thrombocytopenia in neonates are very diverse, and include immune and non-immune disorders. Most cases of thrombocytopenia encountered in the NICU are non-immune, and these will constitute the focus of this review. Specifically, we will first discuss the biological differences between neonatal and adult megakaryocytopoiesis, which contribute to explain the vulnerability of neonates to develop thrombocytopenia. Next, we will review new diagnostic tools that have allowed for a better evaluation of platelet production in neonates, without having to obtain a bone marrow sample. Finally, we will summarize our current understanding of the mechanisms underlying the thrombocytopenia in several common neonatal conditions, such as chronic intrauterine hypoxia, sepsis and necrotizing enterocolitis (NEC), and viral infections. A better understanding of the mechanisms underlying these varieties of thrombocytopenia is critical to develop disease-specific treatment protocols, and to begin to entertain the possibility of using novel thrombopoietic growth factors to treat selected neonates with severe thrombocytopenia.
Thrombocytopenia in hypoxic neonates admitted in NICU is a morbid condition encountered very commonly. Early-onset thrombocytopenia (<72 h) is most commonly associated with fetomaternal conditions complicated by placental insufficiency and/or fetal hypoxia. Chronic intrauterine hypoxia is the most frequent cause of early-onset thrombocytopenia in preterm neonates.
In this study incidence and clinical impact of early thrombocytopenia in hypoxic neonates was investigated.
Setting and Design:
Neonatal intensive care unit of a tertiary level hospital attached to a medical college in Central India. A cross-sectional, observational hospital based study in hypoxic neonates for development of thrombocytopenia.
Materials and Methods:
603 hypoxic newborns were evaluated for development of thrombocytopenia. 155 (25.07%) developed thrombocytopenia and were the cases. Non thrombocytopenic babies 448 (74.29%) served as controls. The two groups were compared for birth weight, sex ratio, gestational age, severity of asphyxia, platelet counts and mortality rate.
Descriptive statistics of continuous variable were expressed in mean and SD. P value less than or equal to 0.05 were statistically significant.
Results and Conclusions:
We found thrombocytopenia to be associated with male gender, prematurity and low birth weight. Most babies had mild to moderate thrombocytopenia. Mortality was higher in preterm thrombocytopenic babies as compared to term. We suggest screening for thrombocytopenia in all asphyxiated newborns, as hypoxia can lead to neonatal thrombocytopenia.
Neonate; birth asphyxia; hypoxia; thrombocytopenia; platelet count
Dengue fever and dengue haemorrhagic fever have emerged as a global public health problem in recent decades. The practice of platelet transfusion has been adapted into the standard clinical practice in management of hospitalized dengue patients. The exact indications and situations in which platelet have to be transfused may vary greatly. Blood components especially platelet concentrates due to their short shelf life are frequently in limited supply. Hence, appropriate use of blood is required to ensure the availability of blood for patients in whom it is really indicated, as well as to avoid unnecessary exposure of the patients to the risk of transfusion reactions and transmission of blood borne infection. The present study was conducted to evaluate the appropriateness of platelet transfusion done in dengue patients with thrombocytopenia. The present study was conducted on 343 serologically confirmed dengue patients admitted at JSS University Hospital between 1st January and 30th August 2009. Clinical data, platelet count and platelet requirements were analyzed. Among the 343 serologically confirmed cases, the prevalence of thrombocytopenia (platelet count < 100,000/cumm) was 64.72% (222 patients) and bleeding manifestations were recorded in 6.12% (21 patients). 71 (20.7%) patients of dengue cases received platelet transfusion. Among them 34 (47.89%) patients had a platelet count <20,000/cumm, 28 patients (39.44%) had platelet counts in the range of 21–40,000/cumm while the remaining 9 (12.67%) patients had platelet count between 41–100,000/cumm. Out of 37 patients with a platelet count >20,000/cumm 11 patients had haemorrhagic manifestations such as petechiae, gum bleeding, epistaxis etc., which necessitates the use of platelet transfusion. However, the remaining 26 patients with platelet count >20,000/cumm and with no haemorrhagic manifestations received inappropriate platelet transfusion. Transfusion of 36.62% of platelet concentrate was inappropriate. The study emphasizes the need for development of specific guidelines for transfusion of blood components, constant interaction and co-ordination amongst clinicians and transfusion centre for implementation of these guidelines and a regular medical audit to review the optimal utilization of blood components.
Dengue; Haemorrhagic fever; Platelet count; Platelet transfusion; Rationale use
The overall prevalence of thrombocytopenia in neonates admitted to neonatal intensive care units ranges from 22 to 35%. There are only a few small studies that outline the relationship between the severity of thrombocytopenia and the risk of bleeding. This makes it difficult to form an evidence-based threshold for platelet transfusions in neonatal patients. The aim of this study was to determine the prevalence of thrombocytopenia in a tertiary neonatal intensive care unit and to study the relation between thrombocytopenia and the risk of intraventricular hemorrhage (IVH).
We performed a retrospective cohort study of all patients with thrombocytopenia admitted to our neonatal tertiary care nursery between January 2006 and December 2008. Patients were divided into 4 groups according to the severity of thrombocytopenia: mild (100-149 × 109/L), moderate (50-99 × 109/L), severe (30-49 × 109/L) or very severe (< 30 × 109/L). The primary outcome was IVH ≥ grade 2. Pearson's chi-squared and Fischer's exact tests were used for categorical data. ANOVA, logistic regression analysis and multivariate linear regression were used for comparisons between groups and for confounding factors.
The prevalence of thrombocytopenia was 27% (422/1569). Risk of IVH ≥ grade 2 was 12% (48/411) in neonates with versus 5% (40/844) in neonates without thrombocytopenia (p < 0.01). After multivariate linear regression analysis, risk of IVH ≥ grade 2 in the subgroups of thrombocytopenic infants was not significantly different (p = 0.3).
After logistic regression analysis the difference in mortality rate in neonates with and without thrombocytopenia was not significant (p = 0.4). Similarly, we found no difference in mortality rate in the subgroups of neonates with thrombocytopenia (p = 0.7).
Although IVH ≥ grade 2 occurs more often in neonates with thrombocytopenia, this relation is independent of the severity of thrombocytopenia. Prospective studies should be conducted to assess the true risk of hemorrhage depending on underlying conditions. Randomized controlled trials are urgently needed to determine a safe lower threshold for platelet transfusions.
Thrombocytopenia is one of the common hematological problems encountered in the neonatal period particularly in the sick newborns, premature babies and neonates admitted in neonatal intensive care units and usually indicate an underlying pathologic process. Thrombocytopenia is reported in neonates with bacterial, fungal, rickettsial, protozoal and viral infection. Some patients with bacterial septicemia may develop coagulopathy associated with DIC. The presence of thrombocytopenia is seen frequently in early sepsis with or without laboratory evidence of overt DIC. This study was conducted on 85 neonates admitted in NICU with clinical diagnosis of septicemia and 50 age and weight matched neonates served as control. Thrombocytopenia was seen in 83.5% cases where as bacterial culture was positive in only 41.1% cases. Further it was noted that, in gram negative (Gm −ve) septicemia, thrombocytopenia was more severe as compared to gram positive (Gm +ve) septicemia. It is concluded that thrombocytopenia is early predictor of septicemia but other causes of neonatal thrombocytopenia should also be ruled out.
Electronic supplementary material
The online version of this article (doi:10.1007/s12288-011-0118-7) contains supplementary material, which is available to authorized users.
Neonatal septicemia; Thrombocytopenia; DIC
Ten cases of isoimmune neonatal thrombocytopenic purpura (4 pairs of siblings and 2 singletons) are described. The condition was diagnosed by excluding other causes of thrombocytopenia , and in 8 cases it was confirmed by detecting antiplatelet antibodies in the mother. Perhaps steroids should be given to affected infants as soon as the condition is diagnosed in order to stabilise the capillary membrane. Exchange transfusion, using platelet antigen-negative blood if available, helps to remove antibodies and should be followed by the infusion of antigen-negative platelets, easily obtained from the mother by platelet-phoresis. The use of random donor platelets (as in 3 of these cases) was ineffective because 98% of the population are platelet antigen-positive. Nine of the infants recovered completely. The exception was an infant who developed hydrocephalus, possibly as a result of intracranial haemorrhage.
Blood group A and B antigens are expressed only weakly on platelets (PLTs) of most individuals but are very strongly expressed on PLTs from approximately 1 percent of normal subjects (Type II high expressers). The implications of this trait for transfusion medicine are undefined.
STUDY DESIGN AND METHODS
A family was studied in which two Group B infants were born with neonatal thrombocytopenia, whereas a third infant whose blood group was A2 had a normal PLT count at birth.
Serologic studies demonstrated a maternal antibody that reacted strongly with PLTs from the father and the two group B children in flow cytometry and with GPIIb/IIIa from their PLTs in solid-phase assays. No PLT-specific antibodies were detected in maternal serum sample, but it contained a high-titer immunoglobulin G antibody specific for blood group B. All PLT-reactive antibody in the mother’s serum was removed by absorption with pooled, washed group A and B red cells (RBCs). Studies with monoclonal anti-B and measurement of serum B-glycosyltransferase activity showed that the father and both group B children were Type II high expressers of blood group B.
The findings indicate that high-titer blood group antibodies acquired from the mother can cause thrombocytopenia in infants possessing the Type II high-expresser phenotype despite competition for antibody binding by blood group antigens expressed on RBCs and other tissues.
The effects of maternal systemic lupus erythematosus (SLE) on neonatal prognosis were examined by comparing clinical features of full-term babies born to lupus mothers and age- and parity-matched controls.
Materials and Methods
From January 2000 to December 2005, 39 singletons were born to 37 SLE women. Excluding 11 cases of prematurity and preeclampsia, 28 full-term neonates formed the lupus group. The control group included 66 full-term babies. The retrospective study examined medical records and compared gestational age, birth weight, days of hospital stay, small for gestational age (SGA) frequency, Apgar scores < 7, and parity. Lupus neonates were tested for anti-nuclear antibody (ANA) and platelet count, and electrocardiogram was performed.
Average gestational age (38 vs. 39 weeks, p < 0.05) and birth weight (2,775 vs. 3,263 g, p < 0.05) were significantly different between the SLE and control groups. SGA frequency was higher in the SLE group (25% vs. 4.5%, p < 0.05). No significant difference was observed in Apgar score, birth weight, gestational age, SGA frequency, and platelet count between lupus subgroups formed based on anti-dsDNA antibody levels and antiphospholipid antibody status.
The association of maternal ANAs, antiphospholipid antibodies, and drug history with neonatal prognosis could not be elucidated. However, even in uncomplicated pregnancies, maternal lupus is disadvantageous for gestational age, birth weight, and SGA frequency.
Lupus erythematosus; systemic; newborn
Thrombocytopenia is frequent among neonates, and 20-25% of affected infants are treated with platelet transfusions. These are frequently given for mild thrombocytopenia (platelets 50-100×109/L), largely due to the known hyporeactivity of neonatal platelets. In tests of primary hemostasis, however, neonates have shorter bleeding and closure times (CTs) than adults. This has been attributed to their higher hematocrits, higher von Willebrand factor (VWF) concentrations, and predominance of longer VWF polymers.
To determine whether the “transfusion” of adult (relatively hyper-reactive) platelets into neonatal blood results in a hypercoagulable profile.
Cord blood (CB) and adult peripheral blood (PB) were separated (using a modified buffy-coat method) to generate miniaturized platelet concentrates (PCs) and thrombocytopenic blood. PB- and CB-derived PCs (n=7 per group) were then “transfused” in-vitro into thrombocytopenic CB and PB. The effects of autologous vs. allogeneic (developmentally mismatched) “transfusions” were evaluated using whole blood aggregometry, platelet function analyzer (PFA-100), and thromboelastography (TEG).
Adult platelets aggregated significantly better than neonatal platelets in response to TRAP, ADP and collagen, regardless of the blood into which they were transfused. The “transfusion” of adult platelets into thrombocytopenic CB resulted in shorter CTs-Epi (PFA-100) and higher clot strength and firmness (TEG), compared to “transfusion” of neonatal autologous platelets.
In vitro “transfusion” of adult platelets into neonatal blood results in shorter CTs than “transfusion” with neonatal platelets. Our findings should raise awareness of the differences between the neonatal and adult hemostatic system and the potential “developmental mismatch” associated with platelet transfusions on neonatal hemostasis.
Hypersplenism due to splenic congestion is observed in portal hypertensive patients. This study was done to know the change in platelets count following early ligation of splenic artery during splenectomy in patients with thrombocytopenia due to portal hypertension with a hypothesis that splenic decongestion results in increased platelets count; thereby platelet transfusion can be avoided.
Materials and Methods:
Patients with platelets count <100,000 per mm3 due to portal hypertension were involved and we followed a protocol of ligating splenic artery first, followed by 30 minutes waiting period for splenic decongestion. Blood sample was collected at 5 and 30 minutes for the estimation of platelets count.
Significant rise in platelets was observed after 5 and 30 minutes of early ligation of splenic artery with mean rise being 23735 ± 15417 and 35085 ± 20458 per mm3, respectively. The rise in platelets at 30 minutes was significant when compared with 5 minutes rise with mean platelets count being 91661 and 103070 per mm3 at 5 and 30 minutes, respectively. The platelets rise was equal to 4 and 6 units of platelets concentrates, respectively.
Early ligation of splenic artery during splenectomy for portal hypertension results in significant rise in platelets after 5 and 30 minutes. This method conserves platelets and avoids platelets transfusion and its complications.
Early splenic artery ligation; platelets count; portal hypertension
Kasabach-Merritt syndrome is characterised by giant haemangioma, thrombocytopenia and coagulopathy. Triggering of disseminated intravascular coagulation along with the need for massive blood transfusion is the major intraoperative complication. A 1-month-old boy was scheduled for excision and split skin grafting of a giant haemangioma over the left thigh. Investigations revealed severe anaemia with thrombocytopenia that was uncorrected despite multiple blood transfusions. Other treatment modalities were also unsuccessful and the neonate was taken up for excision of the haemangioma in order to correct the consumptive coagulopathy. Standard anaesthesia was administered and all appropriate measures to reduce blood loss were instituted. Massive blood transfusion was required but the intraoperative and post-operative period was uneventful and followed by a significant improvement in the haemoglobin and platelet counts in the post-operative period.
Anaesthesia; Kasabach-Merritt syndrome; massive blood transfusion
A 22 year old male presented with breathlessness on exertion, ecchymosis, jaundice and features of worsening right heart failure for the last fifteen days. On physical examination, he had a mid diastolic murmur in the tricuspid area and an ejection systolic murmur in the pulmonary area. Bone marrow histopathology report showed an increased in megakaryocytes count. Routine investigations reports were normal. Echocardiography and computerized tomography (CT) revealed a single mobile large intra cardiac mass originating from the right atrium and causing dynamic obstruction of the right ventricular inflow and outflow tract. Associated fatal thrombocytopenia did not respond to intravenous steroids or platelet transfusion. Patient could not be operated because of very low platelet count, and died during hospital stay before excision biopsy could be done. Pathological autopsy was not done. This is a rare case, as the fatal thrombocytopenia observed here was the result of mechanical effects like frictional and shear force, which can be attributed to the physical presence of a large intra cardiac mass resulting in obstruction to flow.
Frictional force; intra cardiac tumor; mechanical force; shearing force; thrombocytopenia
Three newborn babies with congenital immune amegakaryocytic thrombocytopenia are described. Two were siblings. The mothers' sera showed antibody against both pooled random platelets and lymphocytes of type HLA-A2. Two babies had transient thrombocytopenia and leucopenia and made a full haematological recovery. One baby died aged four hours having had no haematological investigations during life. Histological examination of the bone marrow in all three babies (two by trephine biopsy; one at necropsy) confirmed a deficiency of megakaryocytes. It is suggested that anti-HLA-A2 may cause neonatal thrombocytopenia by depressing megakaryocytes instead of, or in addition to, any direct effect on platelets.
Neonatal alloimmune thrombocytopenia is a rare (1/1000–5000 births) life-threatening disorder, caused by fetomaternal incompatibility for a fetal human platelet alloantigen inherited from the father, with production of maternal alloantibodies against fetal platelets, leading to severe thrombocytopenia and potential bleeding. Intracranial haemorrhage is the most feared complication. This report presents the case of a term newborn infant, born from caesarean section after a normal pregnancy, presenting signs of skin bleeding with different ages. Obstetric history included a previous spontaneous abortion after amniocentesis. Severe thrombocytopenia (4×109/l platelets) was found and brain ultrasound showed multiple intracranial haemorrhages. Human platelet antigen (HPA) phenotyping showed maternal negative HPA-1a and paternal positive HPA-1a platelets. Strongly positive anti-HPA-1a and weakly positive anti-human leukocyte antigen class I alloantibodies were found in the mother. Multiple platelet transfusions, intravenous immunoglobulin and corticosteroid were given but favourable response was accomplished only after a compatible platelet transfusion. Brain MRI showed multiple subacute and chronic haemorrhages.
To determine the risks and benefits associated with the transfusion of packed red blood cells (PRBCs) in extremely low birth weight (ELBW) infants. We hypothesized that when ELBW infants underwent transfusion with the University of Washington Neonatal Intensive Care Unit (NICU) 2006 guidelines, no clinical benefit would be discernible.
We conducted a retrospective chart review of all ELBW infants admitted to the NICU in 2006. Information on weight gain, apnea, heart rate, and respiratory support was collected for 2 days preceding, the day of, and 3 days after PRBC transfusion. The incidence, timing, and severity of complications of prematurity were documented.
Of the 60 ELBW infants admitted to the NICU in 2006, 78% received PRBC transfusions. Transfusions were not associated with improved weight gain, apnea, or ventilatory/oxygen needs. However, they were associated with increased risk of bronchopulmonary dysplasia, necrotizing enterocolitis, and diuretic use (P < .05). Transfusions correlated with phlebotomy losses, gestational age, and birth weight. No association was found between transfusions and sepsis, retinopathy of prematurity, or erythropoietin use.
When our 2006 PRBC transfusion guidelines were used, no identifiable clinical benefits were identified, but increased complications of prematurity were noted. New, more restrictive guidelines were developed as a result of this study.
Human platelet antigens (HPA) are determinant in several platelet-specific alloimmune disorders, such as neonatal alloimmune thrombocytopenia, post-transfusion purpura and platelet transfusion refractoriness. The distribution of HPA systems in the Malaysian population is not known. Defining the patterns of HPA systems provides a basis for risk assessment and management of the above complications.
Materials and methods.
The aim of this study was to investigate the distribution of HPA -1 to -6 and -15 in the three major ethnic groups (Malay, Chinese and Indian) in the Malaysian population. A total of 600 random donor samples, 200 from each of the three ethnic groups, were genotyped by means of real time polymerase chain reaction (PCR) with hydrolysis probes and PCR-restriction fragment length polymorphism (PCR-RFLP).
The most common genotype observed in this study was HPA-1a/1a-2a/2a-3a/3b-4a/4a-5a/5a-6a/6a-15a/15b (17%) followed by HPA-1a/1a-2a/2a-3a/3a-4a/4a-5a/5a-6a/6a-15a/15b (14.33%). The allele frequencies of HPA in Malays and Chinese were found to be similar those of other East and South-East Asian populations, while those of Indians were comparable to the frequencies found in Europeans.
The results of this study have been useful for determining the distribution of HPA polymorphisms in this region and for potential clinical implications.
HPA; genotyping; Malay; Southeast Asia
Polymorphism of human platelet antigens (HPAs) leads to alloimmunizations and immune-mediated platelet disorders including fetal-neonatal alloimmune thrombocytopenia (FNAIT), posttransfusion purpura (PTP), and platelet transfusion refractoriness (PTR). HPA typing and knowledge of antigen frequency in a population are important in particular for the provision of HPA-matched blood components for patients with PTR. We have performed allele genotyping for HPA-1 through -6 and -15 among 998 platelet donors from 6 blood centers in Taiwan using sequence-specific primer polymerase chain reaction. The HPA allele frequency was 99.55, and 0.45% for HPA-1a and -1b; 96.49, and 3.51% for HPA-2a and -2b; 55.81, and 44.19% for HPA-3a and -3b; 99.75, and 0.25% for HPA-4a and -4b; 98.50, and 1.50% for HPA-5a and -5b; 97.75 and 2.25% for HPA-6a and -6b; 53.71 and 46.29% for HPA-15a and -15b. HPA-15b and HPA-3a, may be considered the most important, followed by HPA-2, -6, -1, -5, and -4 systems, as a cause of FNAIT, PTP, and PTR based on allele frequency. HPA-4b and HPA-5b role cannot be excluded based on their immunogenicity. A larger-scale study will now be conducted to confirm these hypotheses and to establish an apheresis donor database for the procurement of HPA-matched apheresis platelets for patients with PTR.
Platelet transfusion is required in the acute phase of some thrombocytopenic disorders in order to prevent potentially dangerous hemorrhages.The purpose of this study was to assess the increase in platelet count following a slow platelet transfusion.
Patients suffering from thrombocytopenia due to various underlying diseases were enrolled in the prospective pilot feasibility trial and were randomly divided into two groups. Standard platelet transfusion was administered in one group, while slow transfusion was used in the other. The platelet count was examined at 1 hour, 24 hours, and 1 week following the transfusions.
Although the platelet count was higher following 1 hour after transfusion via the standard method, the count tended to be higher 1 week after the transfusion in the slow transfusion group. This difference, however, only turned out to be statistically significant amongst females.
A therapy of slow platelet transfusion might be more effective for the prevention of platelet loss. Further studies will be required to strengthen this hypothesis.
Platelet decline; slow platelet transfusion; standard platelet transfusion
Sunitinib is an oral multi-targeted tyrosine kinase inhibitor approved for first line treatment for metastatic renal cell carcinoma and imatinib-resistant metastatic gastrointestinal stromal tumors. Sunitinib administration can cause myelosuppression resulting in neutropenia and thrombocytopenia. Here we present the case of a patient with metastatic renal cell carcinoma who developed sunitinib-induced immune-mediated thrombocytopenia and who was treated with withdrawal of sunitinib and administration of intravenous immunoglobulin and steroids.
This case report describes a 70-year-old Aboriginal Australian with a diagnosis of metastatic renal cell carcinoma. Three weeks after the initiation of sunitinib he developed epistaxis and was admitted with thrombocytopenia (platelets 7 × 109/L) which was found to be refractory to platelet transfusion. Sunitinib was stopped and he was treated with intravenous immunoglobulin and steroids. His platelet count rapidly improved and returned to baseline in three weeks. Only two cases of sunitinib-induced immune-mediated thrombocytopenia have been described in the literature.
Clinicians should have a high index of suspicion for the potential of immune-mediated thrombocytopenia after the initiation of multi-targeted tyrosine kinase inhibitors such as sunitinib. This is a diagnosis of exclusion and can be safely treated by drug withdrawal.
Metastatic renal cell carcinoma; Sunitinib; Thrombocytopenia
Double volume (170 ml/kg body weight) exchange transfusion was done in 52 term infants in the first week of life for neonatal hyperbilirubinemia. The M:F ratio was 1.08:1 and 37 (71.1%) babies were of low birth weight. Causes of jaundice were hemolytic in 46.2% and non-hemolytic in 41.3% cases; in 13.5% babies no cause of jaundice could be found. After exchange transfusion a fall of 14.6% and 47.4% was observed in the hemoglobin and serum bilirubin levels respectively. There was significant (p=0.0414) rise in the mean mid exchange and post-exchange serum sodium levels as compared to pre-exchange values and it was found to be due to higher donor's serum sodium levels (p=0.007). There was no effect on the serum potassium levels during or after ET.
In general serum calcium levels significantly increased at mid-exchange period (p=0.0029) but post-exchange levels were same as pre-exchange. Donor's serum calcium level had no effect on the infant's serum calcium level (p=0.993). There was no change in the serum phosphate and blood urea levels during and after exchange-transfusion. The plasma glucose was significantly raised during and after ET and plasma glucose of the donors had significant effect on the infant's plasma glucose levels (p=0.043). Similarly plasma osmolality also showed significant increase during and after ET which was due to the effect of donor's plasma osmolality (p=0.007).
Gestational diabetes mellitus (GDM) affects up to 10% of all pregnancies and results in significant maternal and neonatal morbidities.
Our main objective was to investigate retrospectively the rate of neonatal intensive care unit (NICU) admissions and significant neonatal complications in pregnant mothers with gestational diabetes.
Materials and Methods:
A retrospective cohort study was conducted. The medical records of King Khalid University Hospital (KKUH) were reviewed from January till December 2007. All pregnant women with GDM along with their offsprings were included and matched with healthy pregnant women. The primary outcome was the rate of NICU admission, hypoglycemia, birth weight and length of hospital stay.
A total of 766 mothers (419 GDM mothers and 347 controls) with their term babies were included. Infants born to GDM mothers had significantly higher risk of NICU admissions [OR 2.7 (95% CI 1.5, 4.9), P value 0.0004], longer hospital stay and higher rates of hypoglycemia. Newborns of GDM mothers had higher rates of perinatal distress and macrosomia; however, the difference did not reach statistical significance.
GDM remains a significant morbidity to newborns resulting in increased intensive care admission, prolongation of hospital stay and higher rates of neonatal hypoglycemia. More efforts to assure early recognition and strict sugar control during pregnancy are still needed.
Gestational diabetes mellitus; hypoglycemia; large for gestational age; macrosomia; neonatal intensive care unit
Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is the commonest cause of severe neonatal thrombocytopenia. FNAIT is usually suspected in neonates with bleeding or severe, unexplained, and/or isolated postnatal thrombocytopenia. Affected fetuses should be managed in referral centers with experience in the ante-natal management of FNAIT. Close collaboration is required between specialists in fetal medicine, obstetrics, hematology/transfusion medicine, and pediatrics. The mother and her partner should be provided with detailed information about FNAIT and its potential clinical consequences, and the benefits and risks of different approaches to ante-natal management. There has been huge progress in the ante-natal management of FNAIT over the last 20 years. However, the ideal effective treatment without significant side effects to the mother or fetus has yet to be determined.
Fetal and neonatal alloimmune thrombocytopenia is a condition that is underdiagnosed.
Immunization seldom occurs in the first pregnancy.
Immunization takes place in association with delivery in most cases.
Anti-HPA-1a level is a predictor for the severity of thrombocytopenia.
intracranial haemorrage; thrombocytopenia; human platelet antigen; transfusion; fetus
Post-transfusion purpura is a rare immunohematological disorder characterized by severe thrombocytopenia following transfusion of blood components and induced by an alloantibody against a donor platelet antigen. It occurs primarily in women sensitized by pregnancy and is most commonly caused by anti-human platelet antigen-1a antibodies. Here, we describe what we believe to be the first documented case of an African-American man who developed post-transfusion purpura due to an anti-human platelet antigen-5b alloantibody after receiving multiple blood products.
A 68-year-old African-American man initially admitted with atrial flutter was started on anticoagulation treatment, which was complicated by severe hematemesis. On days 4 and 5 of hospitalization, he received six units of packed red blood cells, and on days 4, 13 and 14 he received plasma. His platelet count began to drop on day 25 and on day 32 reached a nadir of 7 × 109/L. His platelet count increased after receiving intravenous immune globulin. An antibody with reactivity to human platelet antigen-5b was detected by a solid-phase enzyme-linked immunoassay. Our patient was homozygous for human platelet antigen-5a.
This case emphasizes the importance of including post-transfusion purpura in the differential diagnosis for both men and women with acute onset of thrombocytopenia following transfusion of blood products. The prompt recognition of this entity is crucial for initiation of the appropriate management.
To find the prevalence and causes of thrombocytopenia during pregnancy. An analytical prospective observational study was conducted in Department of Obstetrics & Gynecology, CSMMU, Lucknow. 1079 antenatal women screened for thrombocytopenia and investigated for cause and management strategies and fetomaternal outcome were recorded. Prevalence of thrombocytopenia was 8.8%. Gestational thrombocytopenia was seen in 64.2%, obstetric in 22.1% and medical in 13.68% cases. Mean platelet count in controls was lower with a significant fall (P < 0.001) in the platelet count as pregnancy advanced. Hypertensive and hepatic disorders were the most common obstetric causes of thrombocytopenia. Mode of delivery was not affected by thrombocytopenia. Maternal morbidity and mortality was seen only in medical and obstetric thrombocytopenia. The low platelet counts and declining trend with increasing gestational age predispose Indian women to risk of thrombocytopenia and a routine platelet count is suggested.
Platelet count; Gestational thrombocytopenia; Obstetric thrombocytopenia; DIC; Medical thrombocytopenia; Pregnancy with ITP; Medicine & Public Health; Oncology; Human Genetics; Blood Transfusion Medicine; Hematology