Platelet dysfunction is an early marker for traumatic brain injury-induced coagulopathy.

BACKGROUND: The goal of this study is to determine the presence of platelet dysfunction in patients with traumatic brain injury (TBI). The mechanisms underlying the coagulopathy associated with TBI remain elusive. The question of platelet dysfunction in TBI is unclear. METHODS: This was a prospective observational study conducted at Memorial Hospital of South Bend, IN, and Denver Health Medical Center, CO. A total of 50 patients sustaining TBI, and not under treatment with anticoagulants or platelet inhibitors, were analyzed utilizing modified thromboelastography (TEG) with platelet mapping (TEG/PM), along with standard coagulation tests. RESULTS: Compared to normal controls, patients with severe TBI had a significantly increased percentage of platelet ADP and arachidonic acid (AA) receptor inhibition. Furthermore, the percentage of ADP inhibition distinguished between survivors and non-survivors in patients with TBI (Mann-Whitney test, P = 0.035). ADP inhibition correlates strongly with severity of TBI (Mann-Whitney test, P = 0.014), while AA inhibition did not. CONCLUSION: These data indicate that early platelet dysfunction is prevalent after severe TBI, can be measured in a point-of-care setting using TEG/PM, and correlates with mortality. The mechanism responsible for this platelet dysfunction and associated implications for TBI management remains to be defined.

The use of therapeutic hypothermia after cardiac arrest in a pregnant patient.

Therapeutic hypothermia is an effective intervention for the postresuscitative care of patients who have sustained a cardiac arrest. There has been only 1 documented case of successful resuscitation of a pregnant patient and fetus with therapeutic hypothermia, with an abbreviated developmental follow-up of the child. A 33-year-old woman in her 20th week of pregnancy presented to our emergency department after experiencing a cardiac arrest. After successful resuscitation and a discussion with a multidisciplinary team about expected outcomes, the mother and fetus were successfully treated with therapeutic hypothermia, and a healthy baby was delivered 19 weeks later. The mother's cardiac and neurologic function was normal 36 months after the arrest, and the child has reached all growth and neurodevelopmental milestones. We present a case demonstrating excellent immediate and long-term maternal-fetal neurologic, cardiac, and developmental outcomes after the use of therapeutic hypothermia after cardiac arrest in a pregnant patient.

An unusual cause of dysphagia: pericardial effusion after implantable cardioverter-defibrillator placement.

BACKGROUND: Dysphagia is a known complication of pericardial effusions. Most cases of pericardial effusions are idiopathic, infectious, and neoplastic, but can also occur after cardiac procedures. OBJECTIVE: To report the case of a patient who developed dysphagia from a sub-acute pericardial effusion caused by the placement of an implantable cardioverter-defibrillator (ICD). CASE REPORT: A 62-year-old woman presented to the Emergency Department (ED) with a 2-day history of dysphagia. Imaging revealed a large pericardial effusion compressing the esophagus from the mid-thoracic level to the gastroesophageal junction. Ten days prior, a dual-chamber ICD with small-diameter active fixation leads was placed in the patient. There had been no apparent complications from the procedure, however, over this 10-day period she developed a sub-acute pericardial effusion from an incidental perforation during ICD lead placement that led to the extrinsic compression of the esophagus and her presenting symptom of dysphagia. The patient underwent pericardiocentesis for the pericardial effusion and she was discharged in stable condition. CONCLUSION: This case report highlights the importance of recognizing a non-cardiac complaint such as dysphagia as the primary symptom of a critical cardiac condition. With an increase in cardiac procedures anticipated, clinicians should consider the possibility of a pericardial effusion as a cause of dysphagia, especially for those patients with recent cardiac procedures.

An unruptured, thrombosed 10 cm right coronary artery aneurysm mimicking a pericardial cyst.

Giant coronary artery aneurysms are a rare and potentially life-threatening condition. A 47 year old male presented with a progressive 6 month history of dyspnea and acute right sided chest pain. During the patients work-up, a 10 cm × 10 cm right coronary artery aneurysm was discovered on CT scan and confirmed by cardiac catheterization. The patient was emergently taken to the operating room for aneurysmal resection with placement of a greater saphenous vein bypass graft. There were no post-operative complications and the etiology of this patient's aneurysm was determined to be a congenital ectatic dilation of his right coronary artery. The patient is doing well at 2 years of clinical follow-up.

Haemothorax and thoracic spine fractures in the elderly.

Both osteoporotic fractures and pleural effusions are frequently observed in medicine. However, rarely does one associate a hemorrhagic pleural effusion with a thoracic spinal fracture when the patient has not sustained massive trauma. In this paper, we discuss two cases where seemingly insignificant low-energy trauma precipitated massive haemothoraces in elderly patients with underlying osteoporosis, ultimately resulting in their immediate causes of death. This paper serves to remind health care professionals of the importance of using caution when moving elderly patients as well as to consider thoracic spinal fracture as a potential explanation for a hemorrhagic pleural effusion of undetermined etiology.

Abnormal whole blood thrombi in humans with inherited platelet receptor defects.

To delineate the critical features of platelets required for formation and stability of thrombi, thromboelastography and platelet aggregation measurements were employed on whole blood of normal patients and of those with Bernard-Soulier Syndrome (BSS) and Glanzmann's Thrombasthenia (GT). We found that separation of platelet activation, as assessed by platelet aggregation, from that needed to form viscoelastic stable whole blood thrombi, occurred. In normal human blood, ristocetin and collagen aggregated platelets, but did not induce strong viscoelastic thrombi. However, ADP, arachidonic acid, thrombin, and protease-activated-receptor-1 and -4 agonists, stimulated both processes. During this study, we identified the genetic basis of a very rare double heterozygous GP1b deficiency in a BSS patient, along with a new homozygous GP1b inactivating mutation in another BSS patient. In BSS whole blood, ADP responsiveness, as measured by thrombus strength, was diminished, while ADP-induced platelet aggregation was normal. Further, the platelets of 3 additional GT patients showed very weak whole blood platelet aggregation toward the above agonists and provided whole blood thrombi of very low viscoelastic strength. These results indicate that measurements of platelet counts and platelet aggregability do not necessarily correlate with generation of stable thrombi, a potentially significant feature in patient clinical outcomes.