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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_35_библиотеки_им_акад_М_И_Перельмана

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G. M. Jeha et al.
Several inherited platelet disorders involve abnormalities in platelet enzymes required for normal platelet function. Some examples include deciencies in thromboxane A2 syn­thase, cytosolic phospholipase A2, cyclooxygenase-1, pros­taglandin H synthetase 1, lipoxygenase, glycogen-6 synthetase, and enzymes involved in the metabolism of ade­nosine triphosphate [56, 57].
Diagnosis
Diagnosis of platelet disorders can be challenging. First, it is important to determine whether the patient has a bleeding disorder. Bleeding history is often highly subjective. For example, patients with hereditary bleeding disorders may have not experienced bleeding challenges, while patients without bleeding disorders may exaggerate their symptoms [82, 83]. Occasionally, it is difcult to discern profuse bleed­ing frombleeding in the upper normal range. Secondly, man­ifestation of bleeding disorders may be complicated by patients’ pathophysiological conditions and medication use. Patients without bleeding disorders are still predisposed to bleeding in medical conditions such as cancer, alcohol use disorder, liver disease, kidney disease, connective tissue dis­orders, and hypothyroidism. Medications including but not limited to NSAID, aspirin, glucocorticoid, antibiotics, and SSRI also increase the risk of bleeding. Thirdly, when a bleeding disorder is suspected, it is crucial to determine which component of blood clot formation has been impacted. Platelet dysfunction needs to be differentiated from coagu­lopathy to insure efcacious treatment [84].
In the initial evaluation, physicians should obtain detailed personal bleeding and family history. These include the rea­son for the visit, prior bleeding events, history of bruising or iron deciency, outcome of bleeding challenges, bleeding episodes severe enough for surgical intervention, and men­strual and pregnancy history in female patients [85]. Frequent mucosal bleeding is a sign of bleeding disorder. Excessive menstrual bleeding should raise suspicion because of the high prevalence of bleeding disorders (10–30%) in this pop­ulation of women [85–89]. Incontrast, if a patient did not require transfusion during past hemorrhagic trauma, major surgical procedures, or dental extraction, they are unlikely to havea bleeding disorder. Many institutions employ a stan­dardized bleeding assessment tool (BAT) to evaluate the likelihood of bleeding disorders. BAT generates a bleeding score based on answers to questions about the frequency and severity of epistaxis, cutaneous bleeding, oral cavity bleed­ing, and GI bleeding. A higher score indicates higher risk of bleeding disorder [90, 91].
If a bleeding disorder is suspected after initial history tak­ing and targeted physical exam, a series of laboratory tests is usually employed to determine whether the abnormality is caused by platelet insufciency/dysfunction (primary hemo-
static defect) or by coagulopathy (secondary hemostatic defect). Patients usually rst receive tests including platelet count (normally 150−450×103/mL), morphology, activated partial thromboplastin time (30–40seconds), and prothrom­bin time (9.5–13.5seconds). Abnormality in platelet count and/or morphology can be reviewed from complete blood count. Skin bleeding time test was previously employed to assess platelet disorders; however, it is no longer commonly used because the results are poorly reproducible. Platelet function analyzer (PFA-100), as a replacement to bleeding time, simulates primary hemostasis of blood vessels in response to shear stress and is particularly sensitive to defects in von Willebrand factor [84, 92]. Von Willebrand disease (vWD) is the most common inherited bleeding disorder. It can be diagnosed with PFA-100 in conjunction with vWF activity and vWF antigen levels. It should be noted that in a rare type 2N vWD, factor VIII levels may be very low and the PFA-100 is normal; in type 2B vWD, patients may have varying degrees of thrombocytopenia.
Although PFA-100 is a useful tool to detect vWD, it has a poor sensitivity to many other platelet dysfunctions. Instead, platelet aggregation studies using light transmission aggregometry (LTA) have been widelyimplemented used in the diagnosis of platelet disorders [84]. Platelet aggregation is triggered by theaddition of agonists (e.g., ADP, collagen, epi­nephrine, and thrombin), which causes the platelets to pre­cipitate from solution. As a result, the turbidity of the solution decreases and allows increased light transmission. Light transmission is proportional to the extent of platelet aggrega­tion induced by an agonist [93]. Application of specic ago­nists helps identify the underlying diseases. For example, in Glanzmann thrombasthenia due to defect in GPIIb-IIIa com­plex, platelets will only agglutinate in response to ristocetin; in Bernard-Soulier syndrome caused by adefect in GPIb-IX complex, platelets will aggregate in response to thrombin, collagen, epinephrine, and ADP, but not ristocetin.
Upon observation of abnormalities in the tests mentioned above, further investigation, if available, can be conducted with fresh blood samples. However, these tests can be expen­sive, time-consuming, andproduce results that are depen­dent on the age of the samples. One example is ow cytometry with specic antibodies against important surface receptors (e.g., GPIIb/IIIa, GPIb/IX/V, GPIa/ IIa, and GPIIIb) and/or intra-platelet molecules that are crucial in aggregation signaling pathways. Flow cytometry provides both qualitative and quantitative analysis of platelet aggrega­tion and thus helps to detect the specic defected molecules resulting in aggregation dysfunction [94]. Another example is transmission electron microscopy (TEM), which may be used to uncover the ultrastructure of platelet granules (alpha and delta granules) if apatient issuspected of having a plate­let storage pool disease such as Chediak-Higashi syndrome or Hermansky-Pudlak syndrome [95]. Otherwise, these patients often present with normal platelet aggregometry and
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PFA- 100 results. TEM also helps with diagnosis of the non­muscle myosin heavy chain 9 (MYH9)-related disorders (i.e., May-Hegglin anomaly, Fechtner syndrome, Epstein syndrome, and Sebastian syndrome). Besides TEM, the con­tent and secretion of platelet granules can also be evaluated by ELISA and luminometry based on release products such as platelet factor 4, PDGF, ATP/ADP, and serotonin [96]. Platelet adhesion and spreading disorders can be detected by adhesion and spreading tests, respectively. Surfaces made of different materials (e.g., collagen, brinogen, siliconized glass, and subendothelial matrix) serve to evaluate platelet adhesion function. Observation of platelet size and volume with light microscopy provides information about platelet spreading [84]. Finally, many platelet function disorders are inherited diseases. Therefore, genetic testing has been gain­ing popularity in the diagnosis of known platelet function disorders [97].
Management
There are several options to manage patients with platelet dysfunction disorders who have bleeding. This can vary from conservative management to drug therapy and platelet transfusions. Appropriate treatment depends on several fac­tors including the causative agent, type of platelet disorder, severity of bleeding, and whether or not the patient is planned for an invasive procedure. A careful review of the patient’s medical history is tantamount toward treatment. In general, the initial approach should involve identifying and removing any extrinsic causes of the thrombocytopathy. This could be the removal of certain medications or alteration in a patient’s diet. In other cases, such as inherited or acquired platelet dis­orders, response to treatment can vary. In this section, we will discuss management and treatment of bleeding compli­cations in patients with platelet disorders.
Desmopressin
thrombocytopenia. Because of this variation, it can be useful to give a trial dose. The side effect prole of this medication can vary and includes headache, ushing, blood pressure changes, hypersensitivity reaction (bronchospasm, fever, rash), uid retention, and/or hyponatremia, which could increase the risk of seizures [
53, 98].
Platelet Concentrates
Platelet concentrates concentrations are generally reserved for patients who have a defect in the production or consump­tion of platelets. Platelet concentrates are also used for patients who do not respond to desmopressin or those who experience severe bleeding complications after surgery/ trauma.
Considering this, there are specic indications to theuseof platelet concentrates. Platelet transfusions should be given to patients who suffer from bleeding complications secondary to Glanzmann thrombasthenia or Bernard–Soulier syndrome [5, 53, 98]. These platelet disorders are generally not responsive to desmopressin. A second indication is emer­gency therapy of bleeding for patients who have a defect in megakaryopoiesis or have an increase in platelet turnover secondary to DIC, liver disease, or immune thrombocytope­nic purpura. A third indication is thrombocytopenia postmassive blood transfusion. The nal indication for plate­let transfusionis prophylaxis in patients determined to have high bleeding risk preoperatively [53, 98].
One unit of platelets contains approximately 2–4×10 platelets and in a normal response increases the platelet count by 20,000–30,000/μl in a 70kg adult. For newborns and children, a10ml platelet concentrate/kg body weight is recommended. In general, patients can be given platelets prophylactically if their platelet count is below 5000/μl. However, if a patient has a superimposed qualitative defect, then platelet transfusion should be initiated at a platelet count above 20,000/μl [53].
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Desmopressin is an analog to vasopressin. This medication is known to shorten bleeding time and decrease blood loss. Desmopressin induces the release of vWF from vascular endothelial cells which enhances platelet adhesion to the vessel walls [5]. It can be administered intravenously, subcu­taneously, or as a nasal spray (Octostim) [53, 98]. The rec­ommended parenteral dose is 0.3 micrograms/kilograms of body weight and the intranasal dose is 300 micrograms. It has been shown that desmopressin can shorten bleeding times in storage pool deciencies among other thrombocyto­pathies. However, desmopressin response can be limited especially for patients with Glanzmann thrombasthenia or Bernard–Soulier syndrome [53, 98]. Furthermore, desmo­pressin does not shorten bleeding time in patients with
Recombinant Activated Factor VII (rFVIIa)
Recombinant activated Factor VII is used for bleeding that cannot be treated by conventional means. It has been reported to be effective in patients with Glanzmann thrombasthenia and Bernard-Soulier syndrome for treatment ofbleeding and in surgical intervention. Poon etal. determined that giving prophylactic rFVIIa was effective in 29 out of 31 patients with Glanzmann thrombasthenia [53]. rFVIIa is a via­ble alternative for patients who previouslydeveloped anti­bodies to platelet transfusions. In Europe, rFVIIa has been approved for patients with antibodies against GPIIb/IIIa and/ or HLA and for those patients who do not respond to platelet transfusion [53].
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Dosing includes a minimum of 3 bolus injections of 80–120μg/kg body weight every 1.5–3hours until hemosta­sisis achieved. This regiment has been shown to treat bleeding complications in patients with storage pool diseases, Bernard­Soulier syndrome, and several acquired platelet disorders. A single bolus of 270g/kg has also been shown to be effective. Prior studies indicate that rFVIIa can be effective even when platelet counts are below <20,000/μl. However, it is more effective with higher platelet counts. Frequent administration of rFVIIa is recommended in patients who are less than 12hours from theonset of acute bleeding episode [5, 53].
Antibrinolytics
Antibrinolytics such as aminocaproic acid and tranexamic acid are used to prevent further degradation of blood clots and therefore prevent rebleeding [98]. They are generally used to treat mucocutaneous bleeds, menorrhagia, or gastro­intestinal bleeding. Antibrinolytics combined with cryo­precipitate is the preferred treatment of von Willebrand disease. It can be given orally with a regiment of 2–3 times per day at a total of 1000–1500 mg daily. It can also be given intravenously or be made into a solution and placed on the mouth or nose. A known disadvantage to this medica­tion is that it must be given frequently as bioavailability can be as low as 30% [98].
Hormonal Therapy
Birth control pills can be an option to control bleeding espe­cially in women with signicant menstrual bleeding. Another option is an intrauterine device that releases progesterone. This has been effective in women with bleeding disorders who have heavy menstrual bleeding.
Treatment ofNosebleeds
Nose bleeds can be treated by local measures. One method is to have the patient sit with their head tilted forward while pinching the soft part of their nose for 10minutes untilthe bleeding stops. Individuals can apply petroleum jelly or propylene glycol to prevent drying of mucous membranes. Fibrin sealants containing brinogen, throm­bin, factor XIII, and aprotinin can be used if bleeding is prolonged [98].
Bleeding Associated withMenstruation andChildbirth
Patients with heavy menstruation can use desmopressin, rFVIIa, and antibrinolytics. These products are effective when used at the beginning and during each menstrual
period. IUDs or birth control are used for long-term management [98].
For women who are pregnant are recommended to discuss a delivery plan with their physician. Approaches to bleeding can vary and depend on the specic platelet disorder, the per­son’s experience with past bleeding, and whether delivery will be caesarian or vaginal. It is important to note that bleed­ing risk is elevated right after delivery and several weeks postpartum.
Dental Extraction
Individuals with platelet disorders undergoing dental extrac­tion should be administrated desmopressin as part of their management. It should also be given to the patient prior to receiving a mandibular block which presents a bleeding risk. It is recommended that platelet function be corrected by des­mopressin or another alternative before using performing amandibular block. Antibrinolytic therapy has been shown to reduce bleeding complications following tooth extraction and surgery. Timing is important when using these medica­tions and should be initiated prior to surgery and continued for several days. Lastly, brin glue can be applied to the sur­gical siteintraoperatively [98].
Medications toAvoid
Certain medications can cause platelet dysfunction and should be avoided if possible. Aspirin is commonly used as an antiplatelet medication. It irreversibly inhibits platelet cyclooxygenase impairing thromboxane A2. A dose of 200mg is known to double bleeding time and can produce effects for as long as 4–10 days. Other NSAIDS such as phenylbutazone, indomethacin, fenoprofen, and ibuprofen have also been implicated [5].
Warfarin or heparin is commonly used and may worsen bleeding in these patients. Heparin in particular can cause heparin-induced thrombocytopenia. Antibiotics thathave also been implicated in disruption of hemostasisinclude carbeni­cillin, ticarcillin, penicillin G, ampicillin, and cephalosporin.
Nutraceuticals andFoods toAvoid
Patients with thrombocytopathies should avoid certain foods, additives, and herbal products. These include alcohol, Chinese black tree fungus, ajoene (acomponent of garlic), feverfew, saw palmetto, and various plantbarks.
There are several options for management of complicated bleeding in individuals who have platelet function disorders.
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The approach depends on the offending agent (i.e., food, medications, etc.), the specic platelet disorder, severity of bleeding, andwhether or not the patient is scheduled for an invasive procedure. Based on these factors, treatments can be conservative or may require medications and/or platelet transfusions. It is important to know the indications as well as the side effects of these treatment options, especially of agents such asdesmopressin. Most patients with a platelet dysfunction disorder will not require regulartreatment but may need medical management when determined to be at risk for bleeding complications.
Intraoperative Considerations
Type ofSurgery andProphylactic Treatments
Intraoperative bleeding disturbances can occur secondary to direct surgical manipulation of anatomy or due to hemo­static abnormalities [99]. Hemostatic abnormalities can be present at baseline or arise as a consequence of physiologic and pharmacologic changes associated with the periopera­tive period [99]. Baseline hematologic abnormalities, such as inherited platelet function disorders, present signi­cantly higher intraoperative bleeding risk than inherited platelet number disorders [100]. There does not appear to be a linear relationship between platelet count and risk of spontaneous surgical bleeding, making this serious compli­cation difcult to predict [101]. The Surgery in Platelet Disorders and Therapeutic Approach (SPATA) study showed that type of disorder impacts surgical bleeding risk, with biallelic Bernard-Soulier syndrome being associated with the highest occurrence of perioperative bleeding [100]. Bleeding history and sex are also determining factors of surgical bleeding risk, with female sex being associated with higher bleeding frequency [100]. Cardiovascular and urological surgery is associated with the highest incidence of intraoperative bleeding [100]. Use of laparoscopic ver­sus open approaches and prophylactic establishment of access with two large-bore intravenous catheters have been shown to decrease frequency of hemostatic complications even in high-risk surgeries. Interestingly, the SPATA study demonstrated that the use of pro-hemostatic treatments as pre-operative prophylaxis decreases bleeding frequency in patients with inherited platelet function disorders but not inherited platelet number disorders [100]. Considering the substantial perioperative bleeding risk associated with inherited platelet disorders alone, prophylactic pre-opera­tive pro-hemostatic treatments appear to be vital to decreas­ing bleeding incidence [100].
Traditionally, platelet transfusions have been used at
the highest frequency in patients with established high
bleeding risk [100]. While prophylactic platelet transfu­sions have been shown to decrease rates of clinically sig­nicant bleeding, they have not improved patient outcomes, decreased perioperative RBC requirements, or demonstrated overall mortality benet [101]. Over time, platelet transfusions have been shown to be associated with signicant negative outcomes such as higher rates of postoperative ICU admission and longer hospital stays [101]. In patients who experience acute spontaneous pri­mary intracerebral hemorrhage while on antiplatelet ther­apy, platelet transfusions were associated with enlargement of hemorrhage and increased rates of infection [101]. Platelets have the highest risk of bacterial sepsis of any blood product [101]. Platelet transfusion has also been associated with transfusion-associated acute lung injury, immunomodulation, post-transfusion purpura, and allo­immunization [101]. These observations have paved the way for alternative prophylactic and reactive therapies such as desmopressin, antibrinolytic agents (epsilon aminocaproic acid and tranexamic acid), procoagulant bypass agents (recombinant factor VIIIa and activated prothrombin complex concentrates), and thrombopoietin receptor agonists (romiplostim, eltrombopag, avatrom­bopag, and lusutrombopag), whose mechanisms have been described above [101]. Of note, thrombopoietin receptor agonists are currently used off-label except in patients with thrombocytopenia secondary to chronic liver disease [101].
Anesthesia andAnticoagulation
It has been demonstrated that anesthetic agents have the capacity to inuence hemostasis [99]. In vitro, ketamine dose dependently inhibits platelet aggregation via action on platelet inositol 1,4,5-triphosphate formation, guanosine 5-triphosphatase activity, and calcium currents [99]. Inhibition by ketamine is most notable at doses that exceed concentrations used in clinical settings. This mechanism is important given that the specic effects of anesthetics on platelet function are poorly understood [99]. Anesthetic effects on platelets are difcult to evaluate because measure­ment of platelet function proves challenging [99]. At present, techniques such as bleeding time, platelet aggregometry, and thromboelastography can be used for measurement of plate­let function, but there is no gold standard for accuracy and ease of use [99]. To this extent, platelet aggregometry has shown that not only ketamine but the majority of anesthetic agents including halothane and sevourane inhibit platelet function [99]. Propofol has been consistently associated with signicant platelet inhibition [99]. Unfortunately, there are no data indicating that any one general anesthetic regimen is
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best for reducing perioperative bleeding [99]. So far, basic science reports have brought to the attention of clinicians the potential of hemostatic complications secondary to different anesthetics. Further investigation is needed to determine true clinical impact and the inuences of genetic factors and peri­operative conditions.
Temperature Regulation andtheCoagulopathy ofHypothermia
Intraoperative hypothermia can be caused by a combina­tion of multiple factors occurring simultaneously [102]. Upon entering the operating room, low ambient tempera­tures begin to externally cool the patient [102]. Following induction of anesthesia, the threshold at which the body perceives hypothermia drops from 37.5° to 34.5° [102]. Consequently, the body inappropriately initiates vasodila­tion, decreasing core temperature, and redistributing heat to the extremities [102]. As heat is continually lost due to the cold ambient temperature of the operating room, sur­face area of exposure during surgery is directly related to the amount of heat loss through convective and radiative pathways [103]. Heat loss further contributes to the depression of overall body temperature [103]. At approxi­mately 34.5°C, the brain reinitiates thermoregulative con­trol andinduces vasoconstriction to protect against further core heat loss; however, this vasoconstriction occurs at the expense of the extremities, which continue to see decreasing temperatures [103]. Hypothermia can have a catastrophic effect on the coagulation cascade due to reexive release of thromboxane A3 [104, 105]. This reversible impairment of platelet plug formation com­bined with the reduced coagulation cascade enzyme activ­ity seen in hypothermic patients increases bleeding risk [104, 105]. A lethal triad of hypothermia, acidosis, and coagulopathy is seen in patients with traumatic injuries— in these cases the ineffectiveness of brinogen is explained through both hypothermia and acidosis mechanisms. Hypothermia prevents brinogen synthesis through a decrease in metabolic rate and acidosis causes an increase in degradation due to a pH that is incompatible with enzyme activity, together depleting the amount of brino­gen available and causing coagulopathy [104, 105]. One meta-analysis showed that these mechanisms combine in hypothermic patients to cause a 20% increase in periop­erative blood loss [106]. To combat hypothermia, upper and lower body forced-air warming devices for exposed skin and uid warming devices for refrigerated blood product infusions should be liberally used to maintain normothermic temperatures that encourage adequate clot­ting capacity [105].
Postoperative Blood Loss andTransfusion Requirements
In the case of perioperative or postoperative blood loss, transfusion algorithms have been proposed to combat depressed clotting factors and hypovolemic shock without over-transfusing patients [105]. Intraoperatively, the most current transfusion protocol recommendations include send­ing the following labs every 30minutes: PT/PTT, brinogen, CBC, ABG, and ROTEM [105]. Recommendations also include correction of a hemoglobin less than 7g/dL, a plate­let count less than 50,000, a brinogen level less than 200mg/dL with a double dose given if the brinogen dips under 150mg/dL, and a PT/INR greater than 150% of base­line [105]. If more than four units of packed RBCs are required to restore the hemoglobin concentration, it is rec­ommended to follow a balanced resuscitation protocol that provides balanced units of blood cells and plasma with added platelets and cryoprecipitate. This transfusion protocol is usedfor non-traumatic patients and should not replace the accepted 1:1:1, pRBC:FFP:platelets protocol used in trau­matic settings. These protocols offer more precise, guided treatments for non-traumatic settings of coagulopathic blood loss with the goal of replenishing the patient in a more bal­anced, physiologic manner that includes transfusion ofplate­lets and brinogen more liberally than in otheralgorithms.
The type of procedure must also be consideredin choos­ing a transfusion protocol; certain procedures inherently pro­vide more coagulopathic risk [107]. When platelet count and function were examined in patients undergoing coronary car­diac surgery, platelet count and function were both found todecrease during cardiopulmonary bypass, which increased overall postoperative bleeding and transfusion requirements [107]. Due to the complexity of cardiac patients, an individu­alized algorithm has been established that varies slightly from the above recommendations; the main differenceshere include more aggressive brinogen correction that is recom­mended to occur before addressing other abnormalities [105].
Summary & Conclusion
Alteration in platelet number and function affects the body’s clotting abilities. Platelet disorders can be inherited or acquired defects, which manifest as quantitative or qualita­tive abnormalities. Increased platelets (thrombocytosis and thrombocythemia) will increase the chances of a clot form­ing while decreased platelets (thrombocytopenia) will impair initial plateletplug formation. Altered platelet function with respect to adhesion, receptor function, secretion, enzyme activity, or signaling pathways can also contribution to dys-
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functional formation of the platelet plug. Without adequate formation of the platelet plug individuals tend to experience increased bleeding, purpura, epistaxis, and mucocutaneous bleeding. It is important to differentiate these signs from those of the coagulopathies so that a platelet disorder can be identied and adequatehemostasiscan be promoted.
Evaluation for a platelet disorder typically starts with the history and physical exam. A bleeding assessment tool (BAT) may also be included to screen for a bleeding disorder. If a bleeding disorder is suspected, then more formal testing can be done. Initial workup typically involves a complete blood count and light microscopy to assess platelet count and mor­phology. Coagulation studies are also orderedto evaluate for a coagulopathy. Bleeding time has been replaced by aplate­let function analyzer to assess primary hemostasis. Other platelet disorders are typically tested for with light transmis­sion aggregometry, which can detect platelet aggregation when different agonists are added, allowing the evaluator to narrow down the defect. Different surfaces can be used to evaluate platelet adhesion to various molecules in the body. Flow cytometry allows the detection of specic receptor defects once a differential of possible disorders has been established. Transmission electron microscopy, ELISA, and luminometry can all be used to assess platelet granules and secretion function. Finally, genetic testing can be pur­suedwhen an inherited disorder is suspected. Determining whether or nota platelet disorder is present and achieving the diagnosis frequently requires a combination of any of these tests. The approach to making the diagnosis is highly depen­dent on the given situation and the individual history of any given patient.
Once a platelet disorder has been discovered, manage­ment involves removing any identiablecauses, if applica­ble, and initiating treatment tailored to the givenetiology. NSAIDs, heparin, antibiotics, alcohol, and several foods and herbs can all be culprits that contribute to the manifestation of platelet disorders. Administration of desmopressin can cause vasoconstriction to limit blood loss and release stores of vWF in a decient patient. It is also used for bleeding associated with menses, childbirth, and dental extraction. Desmopressin is not helpful in situations where the receptors are defective or inpatients with thrombocytopenia. In these cases, platelet transfusion may be considered. Transfusion is also used in cases of massive loss of platelets, such as thatseen in consumptive disorders, or occasionally inthose determined to beat a high risk of perioperative bleeding. In cases where this is ineffective, or in cases wherethe patient has been sensitized due to previoustransfusions, recombi­nant activated Factor VII has been shown to be effective. Antibrinolytics have shown to be efcacious in mucocuta­neous bleeds and vWD, but the main limiting factor for their useis the requiredfrequency of dosing. Choice of treatment
is largely based on clinical judgment stemming from factors identied during workup.
Platelet disorders are important to consider in the opera­tive setting. Platelet disorders increase the risk of intraop­erative bleeding, with qualitative disorders presenting more risk than quantitative disorders. Preoperative prophylaxis with desmopressin, antibrinolytics, procoagulant bypass­ing agents, and thrombopoietin receptor agonists can be used to reduce the risk of bleeding. Prophylactic platelet transfusions have fallen out of favor due toa high number of associated risks and limited benet. The low transient tem­perature of the operating room combined with lowered ther­moregulative control secondary to anesthesia can lead to perioperative hypothermia. Perioperative hypothermia affects the function of various coagulation enzymes and fac­tors, which can lead to coagulopathy. These effects can be mitigated by using warming devices and warmed uids as needed during the operation. Perioperative labs should be drawn every 30minutes to monitor bleeding risk. Platelets can be given if concentrations fall below 50,000/μL or to maintain balanced physiology during larger blood transfu­sions. The type of surgery, thepatient’s history, and the situ­ation surrounding the operation must all be considered by the clinical anesthesiologist and othermembers of the team when determining appropriate treatment for patients at risk of bleeding.
References
1. Krishnegowda M, Rajashekaraiah V.Platelet disorders: an over-
view. Blood Coagul Fibrinolysis. 2015;26(5):479–91.
2. D’Andrea G, Chetta M, Margaglione M.Inherited platelet dis-
orders: thrombocytopenias and thrombocytopathies. Blood Transfus. 2009;7:278–92.
3. Freson K, Wijgaerts A, van Geet C.Update on the causes of plate-
let disorders and functional consequences. Int J Lab Hematol. 2014;36(3):313–25.
4. Ghoshal K, Bhattacharyya M. Overview of platelet physiology:
its hemostatic and nonhemostatic role in disease pathogenesis. Scientic World Journal. Scientic World Ltd. 2014;2014:781857.
5. Huebsch LB, Harker LA. Disorders of platelet functions.
Mechanisms, diagnosis and management. West J Med. 1981;134(2):109–27.
6. Krishnegowda M, Rajashekaraiah V. Platelet disorders: an
overview. Blood Coagul Fibrinolysis. Lippincott Williams and Wilkins. 2015;26:479–91.
7. George JN.Platelets. Lancet. 2000;355(9214):1531–9.
8. Simon D, Kunicki T, Nugent D. Platelet function defects.
Haemophilia. 2008;14(6):1240–9.
9. Gauer RL, Braun MM. Thrombocytopenia. Am Fam Physician.
2012;85:612–22.
10. Wolfromm A, Dallemagne J. Management of thrombocytopenia.
Rev Med Brux. 2018;39(4):296–301.
11. Ali N, Auerbach HE.New-onset acute thrombocytopenia in hos-
pitalized patients: pathophysiology and diagnostic approach. J Community Hosp Intern Med Perspect. 2017;7(3):157–67.
66
https://t.me/medicina_free
G. M. Jeha et al.
12. Wong EY, Rose MG.Why does my patient have thrombocytope­nia? Hematol Oncol Clin North Am. 2012;26:231–52.
13. Moulis G, Christiansen CF, Darvalics B, Nørgaard M.Prevalence of thrombocytopenia and thrombocytosis upon acute hospital admission to internal medicine units. A cross-sectional study in Denmark. Eur J Intern Med. Elsevier B.V. 2018;57:e34–7.
14. Smock KJ, Perkins SL.Thrombocytopenia: an update. Int J Lab Hematol. 2014;36(3):269–78.
15. Warkentin TE, Warkentin AE. Acquired thrombocytopenia. In: Concise guide to hematology. Oxford, UK: Wiley-Blackwell;
2011. p.154–73.
16. Dewitte A, Lepreux S, Villeneuve J, Rigothier C, Combe C, Ouattara A, et al. Blood platelets and sepsis pathophysiology: a new therapeutic prospect in critical ill patients? In: Annals of intensive care, vol. 7: Springer; 2017.
gov/pmc/articles/PMC5709271/
17. Venkata C, Kashyap R, Christopher Farmer J, Afessa B.Thrombocytopenia in adult patients with sepsis: incidence, risk factors, and its association with clinical outcome. J Intensive Care. 2013;1(1):9.
18. Sarode R, Nagalla S.Recent advances in understanding and man­agement of acquired thrombocytopenia. F1000Research. Faculty of 1000 Ltd. 2018;7.
19. George JN, Aster RH. Drug-induced thrombocytopenia: patho­genesis, evaluation, and management. Hematology Am Soc Hematol Educ Program. 2009:153–8.
20. Patel N, VanDeWall H, Tristani L, Rivera A, Woo B, Dihmess A, etal. A comparative evaluation of adverse platelet outcomes among Veterans’ Affairs patients receiving linezolid or vancomy­cin. J Antimicrob Chemother. 2012 Mar;67(3):727–35.
21. ten Berg MJ, Huisman A, Souverein PC, Schobben AFAM, Egberts ACG, van Solinge WW, etal. Drug-induced thrombocyto­penia: a population study. Drug Saf. 2006;29(8):713–21.
22. Aster RH, Curtis BR, McFarland JG, Bougie DW.Drug-induced immune thrombocytopenia: pathogenesis, diagnosis, and manage­ment. J Thromb Haemost. 2009;7(6):911–8.
23. Reese JA, Li X, Hauben M, Aster RH, Bougie DW, Curtis BR, et al. Identifying drugs that cause acute thrombo­cytopenia: an analysis using 3 distinct methods. Blood. 2010;116(12):2127–33.
24. Pedersen-Bjergaard U, Andersen M, Hansen PB. Drug-specic characteristics of thrombocytopenia caused by non-cytotoxic drugs. Eur J Clin Pharmacol. 1998;54(9–10):701–6.
25. Pedersen-Bjergaard U, Andersen M, Hansen PB.Drug-induced thrombocytopenia: clinical data on 309 cases and the effect of corticosteroid therapy. Eur J Clin Pharmacol. 1997;52(3):183–9.
26. Pedersen-Bjergaard U, Andersen M, Hansen PB. Thrombocytopenia induced by noncytotoxic drugs in Denmark 1968-91. J Intern Med. 1996;239(6):509–15.
27. George JN, Raskob GE, Shah SR, Rizvi MA, Hamilton SA, Osborne S, et al. Drug-induced thrombocytopenia: a sys­tematic review of published case reports. Ann Intern Med. 1998;129:886–90.
28. Von Drygalski A, Curtis BR, Bougie DW, McFarland JG, Ahl S, Limbu I, etal. Vancomycin-induced immune thrombocytopenia. N Engl J Med. 2007;356(9):904–10.
29. Arnold D, Cucker A.Drug-induced immune thrombocytopenia. Post TW, ed. UpToDate. Waltham: UpToDate Inc.
30. Vardiman JW, Arber DA, Brunning RD, Borowitz MJ, Porwit A, Harris NL, et al. The 2008 revision of the World Health Organization (WHO) classication of myeloid neoplasms and acute leukemia: rationale and important changes. Blood. 2009;114(5):937–51.
31. Alimeida JI, Coats R, Liem TK, Silver D, Sobel M.Reduced mor­bidity and mortality rates of the heparin-induced thrombocytope­nia syndrome. J Vasc Surg. 1998;27(2):309–16.
https://www.ncbi.nlm.nih.
.
32. Liebman HA.Thrombocytopenia in cancer patients. Thromb Res.
33. Ghanavat M, Ebrahimi M, Raeemehr H, Maniati M, Behzad
34. Shahrabi S, Behzad MM, Jaseb K, Saki N. Thrombocytopenia
35. Tefferi A, Hanson CA, Inwards DJ.How to interpret and pursue
36. Assinger A.Platelets and infection- an emerging role of plate-
37. Chammard TB, Schepers K, Breurec S, Messiaen T, Destrem AL,
38. Olariu M, Olariu C, Olteanu D. Thrombocytopenia in chronic
39. Jelkmann W.The role of the liver in the production of thrombopoi-
40. Dahal S, Upadhyay S, Banjade R, Dhakal P, Khanal N, Bhatt
41. Chaudhary B, Imam Rabbani S. Thrombocytopenia and its
42. Navon L, Moritz E, Austin C, Wahl M, Aks S, Layden J.The
43. Rahman K.Effects of garlic on platelet biochemistry and physiol-
44. Harrison CN, Bareford D, Butt N, Campbell P, Conneally E,
45. Skoda RC. Thrombocytosis. Hematol Am Soc Hematol Educ
46. Bleeker JS, Hogan WJ. Thrombocytosis: diagnostic evaluation,
47. Santhosh-Kumar CR, Yohannan MD, Higgy KE, al-Mashhadani
48. Griesshammer M, Bangerter M, Sauer T, Wennauer R, Bergmann
49. Coon WW, Penner J, Clagett GP, Eos N. Deep venous throm-
50. Buss DH, Stuart JJ, Lipscomb GE.The incidence of thrombotic
51. Kuku I, Kaya E, Yologlu S, Gokdeniz R, Baydin A.Platelet counts
52. Koscielny J, Ziemer S, Radtke H, Schmutzler M, Kiesewetter
53. Kirchmaier CM, Pillitteri D.Diagnosis and management of inher-
2014;133(Suppl 2):S63.
MM, Shahrabi S.Thrombocytopenia in solid tumors: prognostic signicance. Oncol Rev. Page Press Publications. 2019;13:43–8.
in leukemia: pathogenesis and prognosis. Histol Histopathol. 2018;33:895–908.
an abnormal complete blood cell count in adults. Mayo Clin Proc. Elsevier Ltd. 2005;80:923–36.
lets in viral infection. Front Immunol. Frontiers Media S.A. 2014;5:649.
Mahevas M, etal. Severe thrombocytopenia after zika virus infec­tion, Guadeloupe, 2016. Emerg Infect Dis. 2017;23(4):696–8.
hepatitis C.J Gastrointestin Liver Dis. 2010;19(4):381–5.
etin compared with erythropoietin. Eur J Gastroenterol Hepatol. 2001;13:791–801.
VR.Thrombocytopenia in patients with chronic hepatitis C virus infection. Mediterr J Hematol Infect Dis. 2017;9(1).
causes. Available online www.jocpr.com. J Chem Pharm Res. 2016;8(2):184–9.
public health response to a large poisoning outbreak involving an illicit substance: synthetic cannabinoids contaminated with a long-acting anticoagulant rodenticide, Illinois, March–July, 2018. J Public Heal Manag Pract. 9000;Publish Ah, Publish Ahead of Print.
ogy. Mol Nutr Food Res. 2007;51:1335–44.
Drummond M, et al. Guideline for investigation and manage­ment of adults and children presenting with a thrombocytosis. Br J Haematol. 2010;149(3):352–75.
Progr. 2009;2009:159–67.
thrombotic risk stratication, and risk-based management strate­gies. Thrombosis. 2011;2011:1–16.
SA.Thrombocytosis in adults: analysis of 777 patients. J Intern Med. 1991;229(6):493–5.
L, Heimpel H.Aetiology and clinical signicance of thrombocy­tosis: analysis of 732 patients with an elevated platelet count. J Intern Med. 1999;245(3):295–300.
bosis and postsplenectomy thrombocytosis. Arch Surg. 1978;113(4):429–31.
and hemorrhagic disorders in association with extreme thrombocy­tosis: an analysis of 129 cases. Am J Hematol. 1985;20(4):365–72.
in adults with iron deciency anemia. Platelets. 2009;20(6):401–5.
H, Salama A, et al. [Preoperative identication of patients with impaired (primary) haemostasis. A practical concept]. Hamostaseologie. 2007;27(3):177–84.
ited platelet disorders. Transfus Med Hemother. 2010;37:237–46.
7 Diseases or Conditions ofPlatelet Disorders
https://t.me/medicina_free
67
54. Rao AK. Congenital disorders of platelet function: disor­ders of signal transduction and secretion. Am J Med Sci. 1998;316(2):69–76.
55. Rao AK, Jalagadugula G, Sun L.Inherited defects in platelet sig­naling mechanisms. Semin Thromb Hemost. 2004;30:525–35.
56. Nurden AT, Nurden P.Inherited disorders of platelets: an update. Curr Opin Hematol. 2006;13(3):157–62.
57. Nurden P, Nurden AT.Congenital disorders associated with plate­let dysfunctions. Thromb Haemost. 2008;99(2):253–63.
58. Malik MA, Masab M. Wiskott-Aldrich Syndrome. [Updated 2020 Jun 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.
gov/books/NBK539838/
59. Villa A, Notarangelo L, Macchi P, Mantuano E, Cavagni G, Brugnoni D, et al. X–linked thrombocytopenia and Wiskott– Aldrich syndrome are allelic diseases with mutations in the WASP gene. Nat Genet. 1995;9(4):414–7.
60. Rodriguez V, Nichols WL, Charlesworth JE, White JG.Sebastian platelet syndrome: a hereditary macrothrombocytopenia. Mayo Clin Proc. 2003;78(11):1416–21.
61. Fechtner syndrome: physiologic analysis of macrothrombocytopenia.- PubMed- NCBI.
62. Untanu RV, Vajpayee N.May Hegglin anomaly. StatPearls. 2019.
63. Mhawech P, Saleem A. Inherited giant platelet disorders classi­cation and literature review materials and methods. Am J Clin Pathol. 2000;113:176.
64. Bishop BN, Brady R. Velocardiofacial syndrome. StatPearls.
2019.
65. Berndt MC, Fournier DJ, Castaldi PA.Bernard-Soulier syndrome. Baillieres Clin Haematol. 1989;2(3):585–607.
66. Lanza F.Bernard-Soulier syndrome (hemorrhagiparous thrombo­cytic dystrophy). Orphanet J Rare Dis. 2006 Nov;1:46.
67. Savoia A, Balduini CL, Savino M, Noris P, Del Vecchio M, Perrotta S, etal. Autosomal dominant macrothrombocytopenia in Italy is most frequently a type of heterozygous Bernard-Soulier syndrome. Blood. 2001;97(5):1330–5.
68. Bragadottir G, Birgisdottir ER, Gudmundsdottir BR, Hilmarsdottir B, Vidarsson B, Magnusson MK, etal. Clinical phenotype in het­erozygote and biallelic Bernard-Soulier syndrome– a case control studyle:///Users/johannhauksson/Downloads/Bragadottir_et_al­2015- American_Journal_of_Hematology.pdf. Am J Hematol. 2015;90(2):149–55.
69. Matsubara Y, Murata M, Sugita K, Ikeda Y.Identication of a novel point mutation in platelet glycoprotein Ibalpha, Gly to Ser at residue 233, in a Japanese family with platelet-type von Willebrand disease. J Thromb Haemost. 2003;1(10):2198–205.
70. Franchini M, Montagnana M, Lippi G. Clinical, laboratory and therapeutic aspects of platelet-type von Willebrand disease. Int J Lab Hematol. 2008;30(2):91–4.
71. Othman M, Notley C, Lavender FL, White H, Byrne CD, Lillicrap D, etal. Identication and functional characterization of a novel 27-bp deletion in the macroglycopeptide-coding region of the GPIBA gene resulting in platelet-type von Willebrand disease. Blood. 2005;105(11):4330–6.
72. Giannini S, Cecchetti L, Mezzasoma AM, Gresele P. Diagnosis of platelet-type von willebrand disease by ow cytometry. Haematologica. 2010;95(6):1021–4.
73. Federici AB. Diagnosis of inherited von Willebrand disease: a clinical perspective. Semin Thromb Hemost. 2006;32(6):555–65.
74. Sadler JE, Budde U, Eikenboom JCJ, Favaloro EJ, Hill FGH, Holmberg L, etal. Update on the pathophysiology and classica­tion of von Willebrand disease: a report of the Subcommittee on von Willebrand Factor. J Thromb Haemost. 2006;4(10):2103–14.
75. Nurden AT.Glanzmann thrombasthenia.
76. Ambrosio AL, Di Pietro SM.Storage pool diseases illuminate platelet dense granule biogenesis. Platelets. 2017;28(2):138–46.
.
77. Sandrock K, Zieger B. Current strategies in diagnosis of
78. Nurden AT, Nurden P.The gray platelet syndrome: clinical spec-
79. Huizing M, Anikster Y, Gahl WA.Hermansky-Pudlak syndrome
80. Gachet C. P2 receptors, platelet function and pharmacological
81. Arthur JF, Dunkley S, Andrews RK. Platelet glycoprotein
82. Wahlberg T, Blomback M, Hall P, Axelsson G.Application of
83. Wahlberg T, Blombäck M, Brodin U. Carriers and noncarriers of
84. Kirchmaier CM, Pillitteri D.Diagnosis and management of inher-
85. Lee CA. Women and inherited bleeding disorders: menstrual
86. Philipp CS, Faiz A, Bowling N, Dilley A, Michaels LA, Ayers G,
87. Trasi SA, Pathare AV, Shetty SD, Ghosh K, Salvi V, Mohanty
88. Woo YL, White B, Corbally R, Byrne M, O’Connell N, O’Shea
89. Kadir RA, Economides DL, Sabin CA, Owens D, Lee
90. Rodeghiero F, Tosetto A, Abshire T, Arnold DM, Coller B, James
91. Tosetto A, Castaman G, Plug I, Rodeghiero F, Eikenboom
92. Jilma B. Platelet function analyzer (PFA-100): a tool to quan-
93. Hvas AM, Favaloro EJ. Platelet function analyzed by light
94. Michelson AD, Barnard MR, Krueger LA, Frelinger AL, Furman
95. Ahnadi CE, Chapman ES, Lépine M, Okrongly D, Pujol-Moix N,
96. Taaning E.Platelet immunology. ELISA for detection of platelet
97. Lentaigne C, Freson K, Laffan MA, Turro E, Ouwehand
inherited storage pool defects. Transfus Med Hemother. 2010;37:248–58.
trum of the disease. Blood Rev. 2007;21(1):21–36.
and Chediak-Higashi syndrome: disorders of vesicle formation and trafcking. Thromb Haemost. 2001;86:233–45.
implications. Thromb Haemost. 2008;99:466–72.
VI-related clinical defects. Br J Haematol. 2007;139(3):363–72.
indicators, predictors and diagnostic indices in coagulation dis­orders. II.Evaluation of laboratory variables with continuous test results. Methods Inf Med. 1980;19(4):201–5.
haemophilia A: I.Multivariate analysis of pedigree data, screen­ing blood coagulation tests and factor VIII variables. Thromb Res. 1982;25:401.
ited platelet disorders. Transfus Med Hemother. 2010;37:3.
issues. Semin Hematol. 1999;36(3 Suppl 4):21–7.
etal. Age and the prevalence of bleeding disorders in women with menorrhagia. Obstet Gynecol. 2005;105:61.
D. The spectrum of bleeding disorders in women with menorrhagia: a report from Western India. Ann Hematol. 2005;84:339.
E, et al. von Willebrand’s disease: an important cause of dysfunctional uterine bleeding. Blood Coagul Fibrinolysis. 2002;13:89.
CA. Frequency of inherited bleeding disorders in women with menorrhagia. Lancet. 1998;351:485.
P, etal. ISTH/SSC bleeding assessment tool: a standardized ques­tionnaire and a proposal for a new bleeding score for inherited bleeding disorders. J Thromb Haemost. 2010;8:2063.
J. Prospective evaluation of the clinical utility of quantitative bleeding severity assessment in patients referred for hemostatic evaluation. J Thromb Haemost. 2011;9:1143.
tify congenital or acquired platelet dysfunction. J Lab Clin Med. 2001;138:152.
transmission aggregometry. Methods Mol Biol. 2017;1646: 321–31.
MI.Evaluation of platelet function by ow cytometry. Methods. 2000;21:259.
Hernández A, etal. Assessment of platelet activation in several different anticoagulants by the Advia 120 hematology system, uorescence ow cytometry, and electron microscopy. Thromb Haemost. 2003;90(5):940–8.
antibodies, platelet-specic antigens and platelet glycoproteins. Dan Med Bull. 1992;39(4):343–54.
WH. Inherited platelet disorders: toward DNA-based diagnosis. Blood. 2016;127:2814.
68
https://t.me/medicina_free
G. M. Jeha et al.
98. Fuse I. Disorders of platelet function. Crit Rev Oncol Hematol. Elsevier Ireland Ltd. 1996;22:1–25.
99. Faraday N. Platelets, perioperative hemostasis, and anesthesia. Anesthesiology. 2002;96(5):1042–3.
100. Orsini S, Noris P, Bury L, Heller PG, Santoro C, Kadir RA, et al. Bleeding risk of surgery and its prevention in patients with inherited platelet disorders. Haematologica. 2017;102(7):1192–203.
101. Nagrebetsky A, Al-Samkari H, Davis NM, Kuter DJ,
102. Sun Z, Honar H, Sessler DI, Dalton JE, Yang D, Panjasawatwong
Kronish JP. Perioperative thrombocytopenia: evi-
Wiener­dence, evaluation, and emerging therapies. Br J Anaesth. 2019;122(1):19–31.
K, et al. Intraoperative core temperature patterns, transfusion requirement, and hospital duration in patients warmed with forced air. Physiol Behav. 2015;122(2):276–85.
103. Kurz A, Sessler DI, Christensen R, Dechert M.Heat balance and distribution during the core-temperature plateau in anesthetized humans. Anesthesiology. 1995;83(3):491–9.
104. Martini WZ. Coagulopathy by hypothermia and acidosis: mechanisms of thrombin generation and brinogen availability. JTrauma- Inj Infect Crit Care. 2009;67(1):208–9.
105. Ghadimi K, Levy JH, Welsby IJ.Perioperative management of the bleeding patient. Br J Anaesth. 2016;117:iii18–30.
106. Reed RL, Johnston TD, Hudson JD, Fischer RP. The dispar­ity between hypothermic coagulopathy and clotting studies. J Trauma- Inj Infect Crit Care. 1992;33:465–70.
107. Adeli EK, Alavi SM, Alizadeh-Ghavidel A, Bakhshandeh­Abkenar H, Pourfathollah AA.Perioperative changes in platelet count and function in patients undergoing cardiac surgery. Med J Islam Repub Iran. 2017;31(1):213–8.
Massive Transfusion Protocol
https://t.me/medicina_free
MaryIm, UsamaIqbal, HongYan, JaimeSanders, andHenryLiu
8
Introduction
Massive transfusion in an adult has commonly been dened as 10 or more units of packed red blood cells (RBCs) in a 24-hour period, which almost replaces one blood volume based on the total blood volume of a 70-kg male [1]. Massive transfusion can also be dened if one of the following condi­tions is satised: blood loss exceeding circulating blood vol­ume within a 24-hour period; blood loss of 50% of circulating blood volume within a 3-hour period; blood loss exceeding 150ml/min; blood loss that necessitates plasma and platelets (PLTs) transfusion [2]. Hemorrhage is the main cause of death in major trauma patients surviving to the hospital admission [3]. In this review, we will discuss the indication of massive transfusion, components and strategies of a mas­sive transfusion protocol (MTP), MTP for specic patient groups, and monitoring performance and outcomes.
Indication ofMassive Transfusion
Perioperative massive hemorrhage can be caused by various etiologies, as illustrated in Table8.1.
M. Im Department of Anesthesiology, Lewis Katz School of Medicine Temple University, Temple University Hospital, Philadelphia, PA, USA
U. Iqbal Department of Anesthesiology, NYU Langone School of Medicine, New York, NY, USA
H. Yan Department of Anesthesiology, Wuhan Central Hospital, Wuhan, Hubei, China
J. Sanders Drexel University College of Medicine, West Reading, PA, USA
H. Liu (
*)
Department of Anesthesiology and Perioperative Medicine, Milton S. Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA
Table 8.1 Etiologies of massive perioperative bleeding [80]
Category Etiologies Surgical procedures Major hepatic surgery
Liver transplantation Cardiac/major vascular surgery Major cancer surgery
Spine surgery Coagulation abnormalities
Obstetric diseases Abnormal placentation
Acute traumatic coagulopathy
Clotting factor deciencies
An undiagnosed inherited bleeding
disorder
Dilutional coagulopathy
Uterine atony
Embryonic emboli-associated DIC
Trauma
Major Trauma is one of the leading causes of perioperative massive hemorrhage and hemorrhage is the main cause of death following major trauma in patients surviving to hospi­tal admission with the highest incidence in 1–3hours after admission [3]. Etiology of major trauma includes motor vehicle accidents, bullet injuries, blunt trauma injuries, fall from certain heights, glass injuries, blast injuries, etc. These traumatic injuries are potentially associated with major vas­cular laceration(s) or organ rupture, leading to extensive blood loss. Most of the patients die on their way to the hos­pital because of massive hemorrhage. Therefore, hemor­rhage with hemorrhagic shock is still the leading cause of death in all major traumatic injuries worldwide [3].
Surgical Procedures
Liver Transplantation
In 1963, Starzl and colleagues performed the rst liver trans­plantation procedure in human being. The rst ve patients all died of bleeding complications [4]. Liver transplantation
© Springer Nature Switzerland AG 2021 C. S. Scher et al. (eds.), Essentials of Blood Product Management in Anesthesia Practice,
https://doi.org/10.1007/978-3-030-59295-0_8
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