deamino-arginine-vasopressin and Brain-Injuries--Traumatic

The authors report permanent central diabetes insipidus (CDI) in a patient after severe traumatic brain injury (TBI) in traffic accident. A 16-year-old boy entered to a medical facility in coma (GCS score 6) with the following diagnosis: acute TBI, severe cerebral contusion, subarachnoid hemorrhage, depressed comminuted cranial vault fracture, basilar skull fracture, visceral contusion. CDI was diagnosed in 3 days after injury considering polyuria and hypernatremia (155 mmol/l). Desmopressin therapy was initiated through a feeding tube. Thirst appeared when a patient came out of the coma after 21 days despite ongoing desmopressin therapy. Considering persistent thirst and polyuria, we continued desmopressin therapy in a spray form. Under this therapy, polyuria reduced to 3-3.5 liters per a day. Symptoms of CDI persisted in long-term period (2 years after TBI) while function of adenohypophysis was intact. This case demonstrates a rare development of permanent diabetes insipidus after TBI. CDI manifested only as polyuria and hypernatremia in coma. Thirst joined after recovery of consciousness. Probable causes of CDI were damage to neurohypophysis and partially injury of pituitary stalk because of extended basilar skull fracture and/or irreversible secondary lesion of hypothalamus following diffuse axonal damage after TBI.. В статье представлен клинический случай развития постоянной формы центрального несахарного диабета (ЦНД) у пациента после тяжелой черепно-мозговой травмы (ТЧМТ) в результате дорожно-транспортного происшествия. Подросток 16 лет поступил в лечебное учреждение в состоянии комы (6 баллов по шкале комы Глазго) с диагнозом: сочетанная травма; острая ТЧМТ; ушиб головного мозга тяжелой степени; субарахноидальное кровоизлияние; вдавленный многооскольчатый перелом свода черепа справа; протяженный перелом основания черепа; ушиб внутренних органов. На 3-и сутки развились полиурия и гипернатриемия (155 ммоль/л); диагностирован ЦНД и начата терапия десмопрессином в таблетированной форме через зонд. При выходе из комы (21-е сутки) отмечено появление жажды на фоне продолжения терапии. В связи с сохраняющейся жаждой и полиурией произведен перевод на терапию десмопрессином в виде спрея, на этом фоне отмечено уменьшение выделения мочи до 3—3,5 л в сутки. Симптоматика ЦНД наблюдалась и через 2 года после ТЧМТ, при этом функция аденогипофиза оставалась сохранной. Представленный случай является примером развития постоянного несахарного диабета у подростка с ТЧМТ, находившегося под длительным наблюдением. Клиническая картина ЦНД в состоянии комы проявлялась только полиурией и гипернатриемией, а по мере повышения уровня сознания присоединилась жажда. Вероятными причинами развития ЦНД явились повреждение нейрогипофиза и частичное повреждение стебля гипофиза в результате протяженного перелома основания черепа и/или необратимого вторичного повреждения гипоталамуса вследствие диффузного аксонального повреждения головного мозга после ТЧМТ.

Topics: Adolescent; Brain Injuries, Traumatic; Coma; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Hypernatremia; Male; Polyuria

Trauma teams are often faced with patients on antithrombotic (AT) drugs, which is challenging when bleeding occurs. We sought to compare the effects of different AT medications on head injury severity and hypothesized that AT reversal would not improve mortality in severe traumatic brain injury (TBI) patients.. An Eastern Association for the Surgery of Trauma-sponsored prospective, multicentered, observational study of 15 trauma centers was performed. Patient demographics, injury burden, comorbidities, AT agents, and reversal attempts were collected. Outcomes of interest were head injury severity and in-hospital mortality.. Analysis was performed on 2,793 patients. The majority of patients were on aspirin (acetylsalicylic acid [ASA], 46.1%). Patients on a platelet chemoreceptor blocker (P2Y12) had the highest mean Injury Severity Score (9.1 ± 8.1). Patients taking P2Y12 inhibitors ± ASA, and ASA-warfarin had the highest head Abbreviated Injury Scale (AIS) mean (1.2 ± 1.6). On risk-adjusted analysis, warfarin-ASA was associated with a higher head AIS (odds ratio [OR], 2.43; 95% confidence interval [CI], 1.34-4.42) after controlling for Injury Severity Score, Charlson Comorbidity Index, initial Glasgow Coma Scale score, and initial systolic blood pressure. Among patients with severe TBI (head AIS score, ≥3) on antiplatelet therapy, reversal with desmopressin (DDAVP) and/or platelet transfusion did not improve survival (82.9% reversal vs. 90.4% none, p = 0.30). In severe TBI patients taking Xa inhibitors who received prothrombin complex concentrate, survival was not improved (84.6% reversal vs. 84.6% none, p = 0.68). With risk adjustment as described previously, mortality was not improved with reversal attempts (antiplatelet agents: OR 0.83; 85% CI, 0.12-5.9 [p = 0.85]; Xa inhibitors: OR, 0.76; 95% CI, 0.12-4.64; p = 0.77).. Reversal attempts appear to confer no mortality benefit in severe TBI patients on antiplatelet agents or Xa inhibitors. Combination therapy was associated with severity of head injury among patients taking preinjury AT therapy, with ASA-warfarin possessing the greatest risk.. Prognostic, level II.

Topics: Aged; Anticoagulant Reversal Agents; Aspirin; Brain Injuries, Traumatic; Cardiovascular Diseases; Comorbidity; Deamino Arginine Vasopressin; Factor Xa Inhibitors; Female; Fibrinolytic Agents; Hemorrhage; Hospital Mortality; Humans; Male; Platelet Transfusion; Risk Assessment; Trauma Severity Indices; Treatment Outcome; United States; Warfarin

Traumatic intracranial hemorrhages expand in one third of cases, and antiplatelet medications may exacerbate hematoma expansion. However, the reversal of an antiplatelet effect with platelet transfusion has been associated with harm. We sought to determine whether a thromboelastography platelet mapping (TEG-PM)-guided algorithm could limit platelet transfusion in patients with hemorrhagic traumatic brain injury (TBI) prescribed antiplatelet medications without a resultant clinically significant increase in hemorrhage volume, late hemostatic treatments, or delayed operative intervention.. A total of 175 consecutive patients with TBI were admitted to our university-affiliated, level I trauma center between March 2016 and December 2019: 54 preintervention patients (control) and 121 patients with TEG-PM (study). After exclusion for anticoagulant administration, availability of neuroimaging and emergent neurosurgery, 62 study patients and 37 control patients remained. Intervention consisted of administration of desmopressin (DDAVP) for nonsurgical patients with significant inhibition at the arachidonic acid or adenosine diphosphate receptor sites. For surgical patients with significant inhibition, dual therapy with DDAVP and platelet transfusion was employed. Study patients were compared with a group of historical controls, which were identified from a prospectively maintained registry and typically treated with empiric platelet transfusion.. Median age was 75 years (interquartile range 85-67) and 77 years (interquartile range 81-65) in the TEG-PM and control patient groups, respectively. Admission hemorrhage volumes were similar (10.7 cm. Among patients with hemorrhagic TBI prescribed preinjury antiplatelet therapy, our study suggests that the use of a TEG-PM algorithm may reduce platelet transfusions without a concurrent increase in clinically significant hematoma expansion. Further study is required to prove a causative relationship.

Topics: Adult; Algorithms; Brain Injuries, Traumatic; Deamino Arginine Vasopressin; Hematoma; Humans; Pilot Projects; Platelet Aggregation Inhibitors; Retrospective Studies; Thrombelastography

BACKGROUND von Willebrand disease (VWD) is characterized by a bleeding tendency due to abnormalities in von Willebrand factor (VWF). Severe traumatic brain injury (TBI) can induce secondary coagulopathy and hemostatic disorders. We herein present a rare case of multiple trauma, including severe TBI, in a patient with VWD who was successfully treated with repeated factor VIII/VWF transfusion in addition to standard critical care. CASE REPORT A 22-year-old man with type 2A VWD sustained head and lower limb injuries in a traffic accident and was comatose. Computed tomography indicated multiple trauma, including severe TBI (left-sided traumatic epidural hematoma, left-sided traumatic subdural hematoma, traumatic subarachnoid hemorrhage, skull fracture, and skull base fracture). The patient underwent emergency craniotomy for hematoma removal, external decompression, and intracranial pressure monitoring along with massive transfusion and repeated perioperative transfusion of factor VIII/VWF concentrates according to the level of bleeding. He recovered consciousness and eventually survived without neurological deficits. CONCLUSIONS Multiple trauma including TBI in patients with VWD is a critical condition. The active transfusion of factor VIII/VWF is essential for controlling hemorrhage early and in the perioperative period.

Topics: Adult; Brain Injuries, Traumatic; Deamino Arginine Vasopressin; Factor VIII; Hematoma; Hemorrhage; Humans; Male; Multiple Trauma; von Willebrand Diseases; von Willebrand Factor; Young Adult

Platelet dysfunction (PD) is an independent predictor of mortality in patients with severe traumatic brain injury (sTBI). Platelet transfusions (PLTs) have been shown to be an effective treatment strategy to reverse platelet inhibition. Their use is contingent on availability and may be associated with increased cost and transfusion-related complications, making desmopressin (DDAVP) attractive. We hypothesized that DDAVP would correct PD similarly to PLTs in patients with sTBI.. This retrospective study evaluated all blunt trauma patients admitted to an urban, level 1 trauma center from July 2015 to October 2016 with sTBI (defined as head abbreviated injury scale [AIS] ≥3) and PD (defined as adenosine diphosphate [ADP] inhibition ≥60% on thromboelastography) and subsequently received treatment. Per our institutional practice, patients with sTBI and PD are transfused one unit of apheresis platelets to reverse inhibition. During a platelet shortage, we interchanged DDAVP for the initial treatment. Patients were classified as receiving DDAVP or PLT based on the initial treatment.. A total of 57 patients were included (DDAVP, n = 23; PLT, n = 34). Patients who received DDAVP were more severely injured (injury severity score, 29 vs. 23; p = 0.045), but there was no difference in head AIS (4 vs. 4, p = 0.16). There was no difference between the two groups in admission platelet count (244 ± 68 × 10/μL vs. 265 ± 66 × 10/μL, p = 0.24) or other coagulation parameters such as prothrombin time, partial thromboplastin time, or international normalized ratio. Before treatment, both groups had similar ADP inhibition as measured by thromboelastography (ADP, 86% vs. 89%, p = 0.34). After treatment, both the DDAVP and PLT groups had similar correction of platelet ADP inhibition (p = 0.28).. In patients with severe traumatic brain injury and PD, DDAVP may be an alternative to PLTs to correct PD.. Therapeutic, level IV.

Topics: Abbreviated Injury Scale; Adult; Blood Platelet Disorders; Blood Platelets; Brain Injuries, Traumatic; Deamino Arginine Vasopressin; Female; Head Injuries, Closed; Hemostatics; Humans; International Normalized Ratio; Male; Middle Aged; Platelet Transfusion; Retrospective Studies; Thrombelastography; Treatment Outcome; Young Adult

There is a high degree of uncertainty regarding optimum care of patients with potential or known intake of oral anticoagulants and traumatic brain injury (TBI). Anticoagulation therapy aggravates the risk of intracerebral hemorrhage but, on the other hand, patients take anticoagulants because of an underlying prothrombotic risk, and this could be increased following trauma. Treatment decisions must be taken with due consideration of both these risks. An interdisciplinary group of Austrian experts was convened to develop recommendations for best clinical practice. The aim was to provide pragmatic, clear, and easy-to-follow clinical guidance for coagulation management in adult patients with TBI and potential or known intake of platelet inhibitors, vitamin K antagonists, or non-vitamin K antagonist oral anticoagulants. Diagnosis, coagulation testing, and reversal of anticoagulation were considered as key steps upon presentation. Post-trauma management (prophylaxis for thromboembolism and resumption of long-term anticoagulation therapy) was also explored. The lack of robust evidence on which to base treatment recommendations highlights the need for randomized controlled trials in this setting.

Topics: Administration, Oral; Anticoagulants; Austria; Brain Injuries, Traumatic; Consensus; Dabigatran; Deamino Arginine Vasopressin; Humans; Interdisciplinary Communication; Partial Thromboplastin Time; Pyrazoles; Pyridines; Pyridones; Rivaroxaban; Thiazoles; Thromboembolism; Tomography, X-Ray Computed; Tranexamic Acid; Treatment Outcome; Vitamin K

The triphasic response of pituitary stalk injury has previously been described in a minority of patients following intracranial surgery, however, this phenomenon can also occur after traumatic brain injury. We present the case of a 20-year-old male who experienced the triphasic response of pituitary stalk injury (central diabetes insipidus, syndrome of inappropriate antidiuretic hormone and central diabetes insipidus again) after striking his head on a concrete curb. His history and presentation highlight the importance of recognising the distinctive symptoms of each individual stage of pituitary stalk injury, and using the appropriate diagnostic tools and therapies to guide further management.

Topics: Antidiuretic Agents; Brain Injuries, Traumatic; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Headache Disorders; Humans; Inappropriate ADH Syndrome; Male; Pituitary Gland; Polyuria; Thirst; Young Adult