Naghma Farooqi, MD, FACOG

• Assistant Professor and Clerkship Director
• Department of Obstetrics and Gynecology
• Texas Tech University Health Sciences Center
• Lubbock, Texas

Anatomic dead space increases because breathed gas does not enter Clinical Evaluation gas exchange units of the lung prostate cancer organization order speman overnight. Physiologic dead space the diagnosis is challenging because symptoms and increases because ventilation to gas exchange units exceeds signs are nonspecific prostate cancer 75 unnecessary operations purchase 60 pills speman amex. Increased pulmonary vascular resistance due to vascular days and that becomes more uncomfortable as time proobstruction or platelet secretion of vasoconstricting gresses prostate 20 grams order 60 pills speman with mastercard. In extreme cases mens health instagram buy 60pills speman mastercard, patients are unable to walk or may require a cane, crutches, or a walker. Sudden, severe calf discomfort suggests a insufficiency due to postphlebitic syndrome. A prominent superficial venous pattern may be evident on the anterior chest wall. Unilateral calf swelling >3 cm 1 Pleuritic chest pain is more common with small periphPitting edema 1 eral emboli. In such cirfiow signal and confirms vein patency proximal and cumstances, clinical improvement often fails to occur distal to Doppler despite standard medical treatment of the concomitant Abnormal response: fiow blunted rather than augmented illness. Perhaps the most frethe quantitative plasma D-dimer enzyme-linked immunosorquent abnormality is T-wave inversion in leads V1 to V4. Elevation of Noninvasive Imaging Modalities D-dimer indicates endogenous although often clinically Venous Ultrasonography ineffective thrombolysis. It appears homopatients with myocardial infarction, pneumonia, sepsis, geneous and has low echogenicity (Fig. The vein cancer, the postoperative state, and second or third itself often appears mildly dilated, and collateral channels trimester of pregnancy. Normally, manual calf compression causes augContrary to classic teaching, arterial blood gases lack mentation of the Doppler fiow pattern. Transthoracic echocardiography rarely images thromPositive Negative bus directly. The most popular nomogram uses an initial bolus of 80 U/kg, followed by an initial infusion rate of Treatment: 18 U/kg per hour. During that period, the parenteral and oral agents ment is needed unless the patient is markedly obese or are overlapped. The dose must be adjusted downward for important adverse effect of anticoagulation is hemorpatients with renal dysfunction because the drug is rhage. The full effect of warfarin requires at least 5 days, even if Major bleeding from warfarin is traditionally manthe prothrombin time, used for monitoring, becomes aged with cryoprecipitate or fresh-frozen plasma (usuelevated more rapidly. The greatest risk of for at least 5 days can counteract the early procoagulant this therapy is rebound thromboembolism. In the setting of percutaneous coronary interassesses the anticoagulant effect of warfarin (Chap. A rare complication is warfarin-induced Proper dosing is difficult because hundreds of drug-drug skin necrosis, which may be related to warfarin-induced and drug-food interactions affect warfarin metabolism. Furthermore, variables such as increasing age and During pregnancy, warfarin should be avoided if poscomorbidities such as systemic illness, malabsorption, sible because of warfarin embryopathy, which is most and diarrhea reduce the warfarin-dosing requirement. However, women can take warfarin dict how individual patients will respond to warfarin. Warfarin dosing can be titrated to results also learns to self-adjust warfarin doses. The latter are polymorphisms can stratify patients into low-, intermecharacterized by clinical stability, absence of chest pain or diate-, and high-dose warfarin groups. An additional shortness of breath, normal right ventricular size and 10% of dosing variance can be explained by allelic varifunction,and normal levels of cardiac biomarkers. There should comorbidities), I recommend standard intensity anticobe a low threshold to initiate these pressors. For patients with preserved systolic blood monary arteries via collateral veins that develop. I concur with these guideParadoxically, by providing a nidus for clot formation, lines. A possible difficult to detect and poses an excessive medical and alternative to open surgical embolectomy is catheter economic burden. New generation catheters are under sures often succeed in preventing this complication development. Patients at high risk can receive a combination of mechanical and pharmacologic modalities. Patients who have undergone if they have initial pulmonary hypertension, it abates total hip replacement, total knee replacement, or cancer over time (usually 6 weeks). Most arterial thrombi Arterial and venous thrombi are composed of are superimposed on disrupted atherosclerotic plaque platelets and fibrin, but the proportions differ. Arterial because plaque rupture exposes thrombogenic material thrombi are rich in platelets because of the high shear in in the plaque core to the blood. In contrast, venous thrombi, which gers platelet aggregation and fibrin formation, which form under low shear conditions, contain relatively few results in the generation of a platelet-rich thrombus that platelets and are predominantly composed of fibrin and can temporarily or permanently occlude blood fiow. Because of the predominance of contrast to arterial thrombi, venous thrombi rarely form platelets, arterial thrombi appear white, whereas venous at sites of obvious vascular disruption. Targeting the components of originate in the valve cusps of the deep veins of the calf thrombi, these agents include (1) antiplatelet drugs, (2) or in the muscular sinuses, where they are triggered by anticoagulants, and (3) fibrinolytic agents (Fig. Sluggish blood fiow in these veins reduces the With the predominance of platelets in arterial thrombi, oxygen supply to the avascular valve cusps. Endothelial strategies to inhibit or treat arterial thrombosis focus cells lining these valve cusps become activated and express mainly on antiplatelet agents, although, in the acute setadhesion molecules on their surface. Platelet recruitment and activation Thrombin generation fibrin is the predominant component of venous thrombi. Antiplatelet drugs are less effective than anticoagulants Platelet aggregation Fibrin formation in this setting because of the limited platelet content of venous thrombi. Vascular injury simultaneously triggers treatment of patients with extensive iliofemoral vein platelet activation and aggregation and activation of the coagthrombosis. Activated platelets potentiate coagulaserves as the foundation of most antiplatelet strategies. In addition to converting fibrinogen to fibAspirin produces its antithrombotic effect by irreversibly rin, thrombin also serves as a potent platelet agonist and acetylating and inhibiting platelet cyclooxygenase recruits more platelets to the site of vascular injury. When rapid X Clopidogrel platelet inhibition is required, an initial aspirin dose of at least 160 mg should be given. Therefore, these administration of proton pump inhibitors may reduce agents also attenuate platelet recruitment. Abciximab, eptifithe risk of aspirin-induced gastrointestinal bleeding in batide, and tirofiban inhibit the final common pathway of patients with peptic ulcer disease. Thus long-term rofecoxib therapy increases aspirin to protect patients from ischemic vascular events. Indications Aspirin resistance has also been described biochemiAspirin is widely used for secondary prevention of carcally as failure of the drug to produce its expected diovascular events in patients with coronary artery, cereinhibitory effects on tests of platelet function, such as brovascular, or peripheral vascular disease.

Complications in Pregnancy: Hypertension and Diabetic Nephropathy in Diabetes in Pregnancy 259 the development of hypertension in nonpregnant subjects with diabetes and patients with diabetes may be associated with microalbuminuria prostate cancer stage 4 speman 60pills amex, the forerunner of overt a slight increase in urinary albumin excrediabetic nephropathy (7) prostate cancer 1cd 10 order speman with a visa. There are four tes mens health magazine uk generic 60 pills speman free shipping, hypertension is closely associated with major hypertensive disorders in pregnancy: an increased risk of cardiovascular disease prostate cancer 38 years old generic 60 pills speman with amex. Each of these diabetes and microalbuminuria or diabetic conditions has unique pathophysiologic nephropathy is of utmost importance to features that have implications for antihyperprevent the progression of kidney disease, tensive therapy (Table 20. Chronic hypertension In women with hypertension early in pregnancy, developing newfionset proteinuria with superimposed fulfills the criteria for preeclampsia. In risk of severe maternal and fetal complicaCopenhagen, a treatment level of chronic tions, such as placental abruption, cerebral hypertension in pregnancy of 135/85 mm/ catastrophe, eclampsia, coagulation abnorHg has been used (9), and even lower treatmalities, abnormal liver function, and even ment levels of 130/80 mmHg for chronic maternal death. Termination of pregnancy is hypertension in diabetic pregnant women are the most effective treatment; therefore, suggested by Kitzmiller and colleagues (1). In addition, imposed preeclampsia often develops earlier women with chronic hypertension are at in pregnancy and with a more severe clinical risk of developing severe hypertension presentation. Preeclampsia is classically defined as development of hypertension later than 20 weeks Practical Aspects of accompanied by proteinuria greater than or equal to 1+ on a sterile urinary dipstick or Detecting Hypertension fi300 mg/24 h. The showed that antihypertensive treatment patient can thereafter be classified as having appeared to reduce the risk of severe hyperhypertension, microalbuminuria, diabetic tension, but no differences were observed in nephropathy, or none of these. Severe Hypertension It is generally accepted that severe hypertenGlycemic Control and Hypertension sion in pregnancy, defined as greater than or Development of preeclampsia is associated equal to 160/110 mmHg, requires treatwith poor glycemic control in both early and ment, because of increased risk of maternal late pregnancy (14,15). Tight glycemic conintracerebral hemorrhage, and treatment trol before and during pregnancy might decreases the risk of maternal death (8,11). Due to the high prevalence of preeclampsia, close monitoring for the Diabetic Nephropathy development of preeclampsia is recomand Hypertension mended in all pregnant women with the prevalence of diabetic nephropathy in diabetes. Most of the literature on this of Hypertension in topic is from women with type 1 diabetes, but the clinical findings are similar in women Pregnancy with type 2 diabetes (20). Women with either microalminuria and 64% in women with diabetic buminuria or diabetic nephropathy prior to nephropathy present before or in early pregpregnancy might even benefit from targeting nancy (9). However, with evidence of microalbuminuria or diasince the majority of these cases lead to betic nephropathy before pregnancy (9). Very similar results have been dysfunction and impaired maximal vasodilaobserved in women with type 2 diabetes (20). There is urinary albumin excretion, tight antihyperusually no deterioration in renal function in tensive treatment during pregnancy should these women during pregnancy. It is imporHowever, longfiterm results are only available tant to obtain and maintain strict glycemic in small patient series (34,36). Complications in Pregnancy: Hypertension and Diabetic Nephropathy in Diabetes in Pregnancy 263 Obstetric Surveillance in Women cardiovascular or central nervous systems with Diabetic Nephropathy (38). In addition to congenital malformations, fetal and neonatal renal failure and oliAround 20 gestational weeks, these women gohydramnios have been observed in women should be offered an ultrasound examination taking these antihypertensives (19,39). In lance, including frequent ultrasound examiparticular, the benefits of discontinuing nations of fetal growth and nonfistress drugs that inhibit the renin angiotensin systesting, is important to diagnose complicatem until pregnancy is confirmed (34,35) tions and plan the time and mode of delivery, must be balanced against the risk of disease with focus on preventing stillbirth as well as progression prior to pregnancy, particularly reducing the prevalence of preterm delivery. Diuretics are commonly prescribed in Hypertension in pregnancy is associated essential hypertension before conception with deterioration of retinopathy (37). Therefore, in pregnant women with diabetic women with microalbuminuria or diabetes and hypertension, screening for diabetic nephropathy is often very salt sensisightfithreatening diabetic retinopathy at tive. In light of this, it may be more approprileast twice, and in selected cases more freate to continue these drugs to avoid the quently, is important based on individual rebound hypertension associated with their evaluation. However, initiating diuretic treatment in women with preeclampsia might reduce placental flow and Choice of Antihypertensive thereby cause fetal hypoxia (17). The alphafiadrenergic agonist thought not to be most common malformations are in the teratogenic based on limited scientific data 264 A Practical Manual of Diabetes in Pregnancy and over 40 years of use in pregnancy. It has antagonists, and other antihypertensive been assessed in a number of trials in pregdrugs, can be used together with magnesium nant women compared with placebo and sulfate, which is used to prevent seizures with alternative antihypertensive drugs (17). In a followfiup study of smooth muscle and has been extensively offspring at 7 years of age exposed to methylused for oral and parenteral treatment of dopa in utero, the children exhibited intellisevere hypertension in late pregnancy, but gence and cognitive development similar to has been replaced by agents with fewer control subjects (17). However, it may have Betafiblockers have been used extensively a place in women resistant to other drugs. Cholesterolfilowering drugs such as statins Intravenous treatment with betafiblockers are contraindicated during pregnancy due to has also been associated with fetal bradytheir possible effects on brain and nerve cardia and hypoglycemia in the newborn development (42). Initiated before 16 gestational weeks, blocker with vascular alphafireceptor blocklowfidose aspirin may reduce the prevalence ing capabilities, has been extensively of preeclampsia in highfirisk women (43). If a monly used to treat chronic hypertension woman is already on lowfidose aspirin treatand preeclampsia. Nifedipine, verapamil, or ment before pregnancy due to increased risk other calcium channel antagonists have of cardiovascular events, continued use durnot been associated with teratogenicity. We, in Nifedipine, the most extensively investigated general, initiate treatment with lowfidose calcium channel antagonist during pregaspirin at 10 gestational weeks. Slowfirelease mins C and E) does not seem to reduce the nifedipine preparations do not have this side prevalence of preeclampsia in women with effect and are widely used for hypertensive type 1 diabetes (45) and is thus not generally disorders in pregnancy (12); calcium channel recommended. Unlike during with diabetes and hypertension are needed pregnancy, methyldopa is, however, not the with a special focus on patients with chronic first choice of antihypertensive therapy during hypertension, microalbuminuria, or diabetic breastfeeding because of adverse effects such nephropathy. Trials comparing the beneficial as fatigue and exacerbation of postpartum effects and side effects of different types of depressive states (46). MultiplefiChoice Questions 1 Which antihypertensive drugs are contrain3 Which statement is correctfi Labetalol) B Development of preeclampsia is C Angiotensinficonverting enzyme associated with poor glycemic coninhibitors trol in pregnancy. D Angiotensin receptor blockers C With careful clinical observation, E Calcium blockers. A Gestational hypertension B Chronic hypertension C Preeclampsia D Superimposed preeclampsia E All of the above Answer: E. Managing preexisting diabetes for hypertension in type 1 (insulinfidependent) pregnancy: summary of evidence and diabetes mellitus. Lessfitight versus tight with long term captopril treatment in control of hypertension in pregnancy. Antihypertensive drug therapy Pressure Education Program Working for mild to moderate hypertension during Group on High Blood Pressure in pregnancy. Report of Improved pregnancy outcome in type 1 the Canadian Hypertension Society diabetic women with microalbuminuria or Consensus Conference: 1. Definitions, diabetic nephropathy: effect of intensified evaluation and classification of antihypertensive therapyfi How to manage hypertension antihypertensive strategy, and pregnancy Complications in Pregnancy: Hypertension and Diabetic Nephropathy in Diabetes in Pregnancy 267 outcome.

It is a combination of laser light scattering and aggregometry to monitor platelet Light-scattering platelet aggregometry [81] microaggregate formation androgen hormone therapy for women 60pills speman with amex. The platelets adhere and aggregate until the aperture is occluded man health store buy speman online from canada, and the time to this closure is recorded prostate cancer 6 on gleason scale buy speman with mastercard. The Plateletworks is a point-of-care test that uses a Coulter counter to measure platelet-count ratio prostate transplant order speman 60 pills with visa, red blood cell count, hemoglobin, and hematocrit. This test uses nonanticoagulated whole blood and can measure several aspects of platelet Clot signature analyzer [86] function and clotting properties. Tromboelastography [87] this device measures clot strength and gives a global assessment of hemostasis. Diagnosis of platelet function relies on clinical fndings In recent times, platelets have emerged to be important markof both detailed medical history and family history. They are multifunctional platelet disorders are hereditary where most of them are blood particles and very important clinical targets for many acquired due to various diseased conditions. Being important infamin platelet function includes prolonged or excessive bleedmatory markers, they play important roles in atherosclerosis ing which is the primary screening procedure to assess and cardiovascular disorders which are correlated with type platelet dysfunction. T eyhaveprofoundroleintumorbiologyas platelet volume are another indicating markers in platelet well as allergic infammation. Obesity is the (v) heavy and prolonged bleeding childbirth, major cause of diabetes in the adults [49]. Finally, monocytes induce migration of endothelial cells, resulting in vascular changes. Tromboxane is induced oxidative stress in structural functional alterations of an important product which plays profound role in platelet hemoglobin and red blood cells [53, 54]. In response to variplasma glucose and HbA1c; higher blood glucose increases ous agonists, hyperaggregation in platelets was reported in the production of TxA2 which is an important product patients with both type 2 and type 1 diabetes mellitus [55, in thromboxane pathway. Hyperaggregation is associated with generating more 11TxA2 production in improved glycaemic controls [58, 62, dehydro-thromboxane B2 which is the important end prod63]. Arachidonic acid Several candidate gene polymorphisms have been associated with platelet functions. TxA2-synthase However, alpha 2 integrin C807T gene polymorphism plays a Tromboxane A (TxA) crucialroleinarterialthrombosis[78]. An explanation of this phenomenon is that larger platelets are more reactive and can 11-Dehydro-TxB2 2,3-dinor-TxB2 express more surface receptors [88, 89]. Moreover a decrease in intracellular Mg concentration platelets is associated with platelet hypersensitivity to diferin diabetic platelets may provoke an accelerating efect in ent agonists [65]. Decreased membrane fuidity of these platelets is as well as production of reduced glutathione. Hyperglycemia attributed to an increased cholesterol-phospholipid molar exerts oxidative stress which can further implement altered ratio in platelet membranes. High fow rates induce conformational changes in vWf allowing interaction of its A3 domain with matrix collagen. Metformin, an oral antidiabetic, frst line lurea derivative, can check blood glucose level by its free drug of biguanide class, is particularly useful for overweight radical scavenging ability. Diferent researchers concluded that metformin endothelial cell adhesion [102, 103]. Hemostasis and thrombosis Maintenance/regulation of vascular tone Adhesion Uptake of serotonin when resting Activation Release of serotonin, thromboxane, prostaglandins Spreading Upon activation Secretion Aggregation Procoagulant activity Clot retraction Tissue repair Platelet functions Infiammation Atherosclerosis Tumor biology Allergic asthma Tumor growth Renal disease Tumor killing Chemotaxis Tumor metastasis Host defense Platelet-leukocyte Phagocytosis/internalisation of viruses interactions and bacteria Killing of bacteria Release of platelet microbicidal proteins Superoxide production Figure 8: The multifunctional platelet (adapted from Harrison, 2005 [44]). Administration of rosiglitazone has signifcantly reduced von Willebrand factor in 4. Platelets from patients with type 2 diabetes inhibiting enzyme glycoside hydrolases. Both intrinsic platelet abnormalities and ciated metabolic syndrome jointly correlate with prothromimpaired platelet-vessel wall interaction can contribute to bic state in diabetes mellitus to put a cumulative efect in the platelet dysfunction [125]. Researchers have identifed a direct correlation between insulin-induced attenuation 5. Platelet plays versatile role in 2+ of the thrombin-induced Ca response and platelet aggregacancer progression. Diabetic platelet shows an altered Ca homeby platelets can secure the coagulation of cancer cells, ostasis [112]. Notonlyfunctionsbutplateletnumbersalsohave platelet activity can give major insights into heart disease and been reported to decrease in liver diseases [140]. Some common pathological features include thrombocytopenia, glomerular Biomarkers are now emerging with immense scientifc and thrombosis, and thrombi in small arteries and glomerular clinical value through the whole journey of the disease 12 The Scientifc World Journal process.

C Fujimori 1999 prostate oncology quality generic 60 pills speman overnight delivery, Bolton-Maggs 2006 For patients with a congenital thrombocytopathy / thrombocytopenia androgen hormone oestrogen discount speman 60 pills overnight delivery, platelet transfusions are only indicated for a procedure or in case of bleeding mens health yahoo answers generic 60 pills speman otc,if medicinal treatment is insufficient mens health 28 day abs buy generic speman 60 pills. Level 3 C Bolton-Maggs 2006, Almeida 2003, Manco-Johnson 2001, 1996, Mannucci 1997, Weiss 1996, Fujimori 1999 Other considerations Allo-immunisation is extremely undesirable in patients with congenital thrombocytopathy or thrombocytopenia, since platelet transfusions may be necessary in the event of severe acute bleeding. For patients with a congenital thrombocytopathy and/or thrombocytopenia the advice is to limit the administration of platelet transfusions as much as possible due to the development of alloantibodies, which can destroy the effect of platelet transfusions. Prophylactic platelet transfusions are not indicated in case of congenital thrombocytopenia and thrombocytopathy. In congenital thrombocytopenia and thrombocytopathy platelet transfusions are indicated for procedures and in case of severe bleeding if other treatment modalities are not effective. In a meta-analysis of these older randomised studies, Stanworth (2004) concluded that there was fewer large and severe bleeding when prophylactic transfusions were given. One observational study of autologous stem cell transplant patients with transient thrombocytopenia only administered therapeutic transfusions. Level 1 A1 Stanworth 2004 A therapeutic transfusion policy may be safe in furthermore healthy patients with transient thrombocytopenia. Wandt et al (Wandt 2006) studied patients following autologous stem cell transplantation: these patients are less sick and have only transient thrombocytopenia compared to the patients from the meta-analysis by Stanworth (Stanworth 2004). A therapeutic transfusion policy can be considered for furthermore healthy patients experiencing a short period of pancytopaenia. Observational 9 cohort studies reported that transfusion triggers lower than 20 x 10 /L did not result in a higher incidence and/or increased severity of bleeding (Slichter 1978, Gaydos 1962, Gmur 1991, Wandt 1998, Sagmeister 1999, Gil-Fernandez 1995, Navarro 1998, Lawrence 2001, Callow 2002, Nevo 2007a). A retrospective analysis of patients treated with a myelo-ablative allogeneic haematopoietic stem cell transplant compared patients who were transfused at a platelet transfusion trigger 9 9 of 10 x 10 /L with a historic group of 170 patients transfused at a trigger of 20 x 10 /L. In the lower trigger group there were significantly more patients with deep thrombocytopenia < 10 x 9 10 /L (19% versus 7%). In both cohorts, deep thrombocytopenia was associated with higher mortality; however, this was not due to bleeding (Nevo 2007). However, it was not demonstrated that increasing the platelet transfusion threshold to 20 x 9 10 /L had any effect on this non-bleeding related mortality. Four randomised studies in patients treated because of a haemato-oncological malignancy 9 9 and/or stem cell transplantation compared transfusion triggers of 10 x 10 /L and 20 x 10 /L 9 9 (Heckman 1997, Rebulla 1997, Zumberg 2002) and 10 x 10 /L and 30 x 10 /L (Dietrich 2005). The same 3 studies (Heckman 1997, Rebulla 1997, Zumberg 2002) were included in the Cochrane analysis in 2004. This meta-analysis concluded that equivalence between a trigger of 10 and 9 20 or 30 x 10 /L had not (yet) been demonstrated (Stanworth 2004). At least 3 analyses of large study populations on the risk of bleeding show that it is not the platelet count but the occurrence of a bleeding in the preceding five days that is the most important risk factor for bleeding. However, in practice, the transfusion 9 threshold is increased to 20 x 10 /L almost everywhere in the case of a severe bleeding. This can be the reason that bleeding occurs primarily at higher platelet counts in these analyses. Blood Transfusion Guideline, 2011 229 229 the optimal threshold level for platelet transfusions has not been examined for patients who are taking anti-coagulant medication. However, the studies were too Level 2 small to conclude that the various triggers are equal. B Rebulla 1997, Heckman 1997, Zumberg 2002, Dietrich 2005 In patients following allogeneic myelo-ablative haematopoietic stem cell 9 transplantation, maintaining a platelet transfusion trigger of 10 x 10 /L was associated with significantly more periods of deep thrombocytopenia than 9 when a platelet transfusion trigger of 20 x 10 /L was maintained (19% Level 3 versus 7%). In both cohorts, deep thrombocytopenia was associated with higher mortality, however, this was not due to bleeding. C Nevo 2007 230 Blood Transfusion Guideline, 2011 In clinical situations that can promote bleeding (sepsis, fever, high blast count, extensive endothelial damage) consensus guidelines advise 9 increasing the platelet transfusion trigger to 20 x 10 /L. The working group deems that the number of platelet triggers 9 should be reduced (namely 10, 20, 50 and 100 x 10 /L), as there is very little evidence 9 supporting the various triggers. Therefore, the current consensus recommends 50 x 10 /L 9 for patients with an indication for anti-coagulant therapy. Although the platelet count does not appear to be related to an increased risk of recurrent bleeding in patients who have experienced severe bleeding in the preceeding 5 days, most experts still feel that for the present it is safer to increase the platelet transfusion trigger to 9 20 x 10 /L for such patients. In the case of a standard risk of bleeding, a transfusion trigger of 10 x 10 /L is recommended for prophylactic platelet transfusions. If there are additional clinical complications that promote bleeding, it is recommended 9 that the platelet transfusion trigger be increased to 20 x 10 /L for prophylactic platelet transfusions. For patients with an indication for anti-coagulant treatment, it is recommended to 9 increase the platelet transfusion trigger to 50 x 10 /L in order to prevent spontaneous bleeding; this is not evidence based. Various randomised studies compared a low, standard and high transfusion dose for prophylactic platelet transfusions (Goodnough 2001, Klumpp 1999, Norol 1998, Sensebe 2005, Tinmouth 2004). A meta11 11 analysis of these 5 studies by Cid in 2007 compared a dose of < 3 x 10 versus > 3 x 10. Blood Transfusion Guideline, 2011 231 231 Use of the higher dose resulted in a significantly longer interval to the next transfusion and a higher post-transfusion value. Since then, two randomised studies have been performed with bleeding as end point. Use of the bleeding time to determine the indication for platelet transfusions during procedures is unreliable (Lind 1991). Thorough preparation for the procedure, checking for medications that interfere with haemostasis, monitoring the level of clotting factors, discontinuing anti-coagulant medication if necessary and avoiding hypothermia of the patient are advised (Bain 2004, Valeri 2007). Mild bleeding was observed at platelet counts < 50 x10 /L, primarily increases in further bleeding of the insertion site (Doerffler 1996, Mumtaz 2000, Ray 1997). The largest series reported no increase in bleeding 9 during ultrasound-guided biopsies, despite a platelet count < 50 x 10 /L, with or without additional clotting abnormalities (Caturelli 1993). High risk operations 9 Various guidelines advise platelet target values > 100 x 10 /L for high risk operations, such as heart, brain or eye surgery (excluding cataract surgery). These target values were not based on comparative research with bleeding as end point. As revision of the recent 9 literature found no indications that more or fewer bleeds would occur at 40 versus 60 x 10 /L 9 and a platelet count of 50 x 10 /L is recommended as trigger/threshold value elsewhere in 9 this guideline, the working group has decided to maintain a platelet count of 50 x 10 /L 9 9 instead of 40 or 60 x 10 /L. Platelet transfusions may be necessary if there is no response or if there is a need for emergency surgery such as a splenectomy. The aim is to achieve a non-traumatic birth, particularly in the interests of the child. The cause of this is a strong reaction by platelet-specific alloantibodies that reach a high titre in a short period of time, with the autologous platelets being broken down as innocent bystanders. This is because it may promote thrombotic complications (Swisher 2009, Harkness 1981; Lind 1987; Bell 1991; Kennedy 2000). Elective procedures should be postponed as long as possible, until treatment of the underlying disease has started. Non-evidence based guidelines advise to aim for > 50 x 10 /L 9 platelets for a Caesarian section and > 20 x 10 /L for a vaginal delivery (Van Dam 1989, Sibai 1990, Sibai 2004, Baxter 2004, Haram 2009).

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