Postmortem noninvasive virtual autopsy: extrapleural hemorrhage after blunt thoracic trauma

A 19-year-old man speeding recklessly along a highway caused a left-frontal crash with another car. After his vehicle came to a standstill, he climbed out of the wreck and crawled across the tarmac to the other side of the road, where he died several minutes after the accident and before the arrival of an ambulance. Postmortem multislice computed tomography (MSCT) demonstrated fractures of the first, second, and third ribs and scapula on the left, an extrapleural hemorrhage in the apical region of the left thorax, as well as a large amount of blood in the left thoracic cavity. These radiologic findings were indicative of a delayed rupture of a traumatic extrapleural hematoma into the pleural space. A traditional autopsy confirmed the very rare diagnosis of a traumatic extrapleural hemorrhage with a delayed rupture.

Hemorrhage in vitamin K deficiency--a preventable entity

Der diaplazentare Transport von Vitamin K ist kaum messbar, die Muttermilch ist arm an Vitamin K und die intestinale Flora von Neugeborenen produziert praktisch kein Vitamin K. Deshalb weisen gesunde Neugeborene «physiologischerweise» tiefe Vitamin-K-Spiegel auf, was durch Verminderung der Vitamin-K-abhängigen Gerinnungsfaktoren zu schweren Mangelblutungen führen kann. Die klassische Form der Vitamin-K-Mangelblutung tritt mit einer Inzidenz von bis zu 1.5% bis zum 7. Lebenstag auf, die Spätform wird bis zur 12. Lebenswoche bei bis zu 10 von 100000 Neugeborenen festgestellt. Mit einer adäquaten Vitamin-K-Prophylaxe lassen sich Vitamin-K-Mangelblutungen grösstenteils verhindern. Die heute in der Schweiz empfohlene Prophylaxe von 3 oralen Dosen à 2 mg Konakion® MM in der 4. Lebensstunde, am 4. Lebenstag und in der 4. Lebenswoche ist bezüglich unerwünschter Nebenwirkung äusserst sicher, insbesondere besteht kein erhöhtes Krebsrisiko. Angesichts der dramatischen Folgen der häufig intrakraniell lokalisierten Vitamin-K-Mangelblutungen ist sowohl bei medizinischen Fachpersonen als auch bei den Eltern eine möglichst gute Compliance für diese einfache und sichere Prophylaxe wie auch eine entsprechende Aufklärung anzustreben.

rFVIIa in the treatment of persistent hemorrhage in pediatric patients on ECMO following surgery for congenital heart disease

BACKGROUND: Patients who require extracorporeal membrane oxygenation (ECMO) postsurgery for congenital heart disease (CHD) frequently experience severe bleeding episodes. Whereas recombinant-activated factor VII (rFVIIa) has proven efficacy in counteracting intractable hemorrhage in various scenarios, its use in patients on ECMO is limited by the increased risk for thrombotic events. METHODS: Between December 2004 and January 2006, ECMO was used in 10 pediatric patients following cardiac surgery, of whom seven were treated with rFVIIa because of intractable hemorrhage. Their medical records were reviewed with respect to variations in chest tube output and transfusion requirements, occlusion of or thrombus formation in the ECMO circuit and the occurrence of thromboembolic events. Outcome and rate of ECMO circuit occlusion were compared with historic controls. RESULTS: Three patients died, and four survived (none of the deaths was attributable to thrombus formation or bleeding). All patients were treated with aprotinin prior to and during rFVIIa therapy. Two patients developed an occlusion of the oxygenator, one after receiving co-medication with a FXIII concentrate, another after RBC transfusion in the ECMO system. In two patients, thrombus formation was observed in the ECMO system on inspection after discontinuation. Thromboembolic events were not observed. CONCLUSIONS: Recombinant-activated factor VII in a median dosage of 90 microg.kg(-1) was used in seven pediatric patients on ECMO. Rates of ECMO system occlusions and mortality did not differ from historic controls. Neither the reduction of chest tube output nor the blood product transfusion requirements did reach statistical significance.

Prior statin use, intracranial hemorrhage, and outcome after intra-arterial thrombolysis for acute ischemic stroke

BACKGROUND AND PURPOSE: There are only limited data on whether prior statin use and/or cholesterol levels are associated with intracranial hemorrhage (ICH) and outcome after intra-arterial thrombolysis. The purpose of this study was to evaluate the association of statin pretreatment and cholesterol levels with the overall frequency of ICH, the frequency of symptomatic ICH, and clinical outcome at 3 months. METHODS: We analyzed 311 consecutive patients (mean age, 63 years; 43% women) who received intra-arterial thrombolysis. RESULTS: Statin pretreatment was present in 18%. The frequency of any ICH was 20.6% and of symptomatic ICH 4.8%. Patients with any ICH were more often taking statins (30% versus 15%, P=0.005), more often had atrial fibrillation (45% versus 30%, P=0.016), had more severe strokes (mean National Institute of Health Stroke Scale score 16.5 versus 14.7, P=0.022), and less often good collaterals (16% versus 24%, P=0.001). Patients with symptomatic ICH were more often taking statins (40% versus 15%, P=0.009) and had less often good collaterals (0% versus 24%, P<0.001). Any ICH or symptomatic ICH were not associated with cholesterol levels. After multivariate analysis, the frequency of any ICH remained independently associated with previous statin use (OR, 3.1; 95% CI, 1.53 to 6.39; P=0.004), atrial fibrillation (OR, 2.5; CI, 1.35 to 4.75; P=0.004), National Institutes of Health Stroke Scale score (OR, 1.1; CI, 1.00 to 1.10; P=0.037), and worse collaterals (OR, 1.7; CI, 1.19 to 2.42; P=0.004). There was no association of outcome with prior statin use, total cholesterol level, or low-density lipoprotein cholesterol level. CONCLUSIONS: Prior statin use, but not cholesterol levels on admission, is associated with a higher frequency of any ICH after intra-arterial thrombolysis without impact on outcome.

Cell replacement therapy for intracerebral hemorrhage

Intracerebral hemorrhage (ICH), for which no effective treatment strategy is currently available, constitutes one of the most devastating forms of stroke. As a result, developing therapeutic options for ICH is of great interest to the medical community. The 3 potential therapies that have the most promise are cell replacement therapy, enhancing endogenous repair mechanisms, and utilizing various neuroprotective drugs. Replacement of damaged cells and restoration of function can be accomplished by transplantation of cells derived from different sources, such as embryonic or somatic stem cells, umbilical cord blood, and genetically modified cell lines. Early experimental data showing the benefits of cell transplantation on functional recovery after ICH have been promising. Nevertheless, several studies have focused on another therapeutic avenue, investigating novel ways to activate and direct endogenous repair mechanisms in the central nervous system, through exposure to specific neuronal growth factors or by inactivating inhibitory molecules. Lastly, neuroprotective drugs may offer an additional tool for improving neuronal survival in the perihematomal area. However, a number of scientific issues must be addressed before these experimental techniques can be translated into clinical therapy. In this review, the authors outline the recent advances in the basic science of treatment strategies for ICH.

Focal laminar cortical infarcts following aneurysmal subarachnoid haemorrhage

INTRODUCTION: The aim of this prospective study was to analyse small band-like cortical infarcts after subarachnoid haemorrhage (SAH) using magnetic resonance imaging (MRI) with reference to additional digital subtraction angiography (DSA). METHODS: In a 5-year period between January 2002 and January 2007 10 out of 188 patients with aneurysmal SAH were evaluated (one patient Hunt and Hess grade I, one patient grade II, four patients grade III, two patients grade IV, and two patients grade V). The imaging protocol included serially performed MRI with diffusion- and perfusion-weighted images (DWI/PWI) at three time points after aneurysm treatment, and cerebral vasospasm (CVS) was analysed on follow-up DSA on day 7+/-3 after SAH. RESULTS: The lesions were located in the frontal lobe (n=10), in the insular cortex (n=3) and in the parietal lobe (n=1). The band-like infarcts occurred after a mean time interval of 5.8 days (range 3-10 days) and showed unexceptional adjacent thick sulcal clots. Seven out of ten patients with cortical infarcts had no or mild CVS, and in the remaining three patients DSA disclosed moderate (n=2) or severe (n=1) CVS. CONCLUSION: The infarct pattern after aneurysmal SAH includes cortical band-like lesions. In contrast to territorial infarcts or lacunar infarcts in the white matter which develop as a result of moderate or severe proximal and/or distal vasospasm visible on angiography, the cortical band-like lesions adjacent to sulcal clots may also develop without evidence of macroscopic vasospasm, implying a vasospastic reaction of the most distal superficial and intraparenchymal vessels.

Ependymoma of conus medullaris presenting as subarachnoid haemorrhage

Subarachnoid haemorrhage (SAH) due to spinal ependymoma is very rare. We report a 37 year old man who presented with typical clinical signs of SAH. Lumbar puncture confirmed SAH but cerebral angiography was negative, and further diagnostic work-up revealed an ependymoma of the conus medullaris as the source of the haemorrhage. A comprehensive review of the literature was conducted. Only 17 patients with spontaneous SAH due to a spinal ependymoma have been reported since 1958. However, in cases of SAH and negative diagnostic findings for cerebral aneurysms or malformations, this aetiology should be considered and work-up of the spinal axis completed.

Acute lower gastrointestinal hemorrhage: minimally invasive management with microcatheter embolization

PURPOSE: To evaluate the efficacy of superselective embolization therapy in the management of acute lower gastrointestinal (LGI) hemorrhage, including any bleeding distal to the ligament of Treitz. MATERIALS AND METHODS: Between June and August 2007, 20 patients with acute LGI bleeding underwent superselective transcatheter arterial embolization (TAE) at the authors' institution. The bleeding had different causes. All patients were treated with use of microcatheters. The following embolic agents were used: microcoils (n = 16), polyvinyl alcohol (PVA) particles (n = 2), and a combination of microcoils and PVA particles (n = 2). Outcome measures included technical success (complete cessation of bleeding as documented at completion angiography), clinical success (resolution of signs or symptoms of LGI bleeding within 30 days after TAE), and the rate of major and minor complications. RESULTS: The identified bleeding sources were as follows: jejunal branch, branch of middle colic artery, branch of ileocolic artery, ileal branch, branch of left colic artery, branch of sigmoid artery, branch of the superior rectal artery, and branch of the middle rectal artery. Technical success with effective control of active bleeding was achieved in all patients (100%). Clinical success attributed to TAE was documented in 18 of the 20 patients (90%). Major complications included death due to pulmonary embolism, heart infarction, and multiorgan failure in the 3rd week after TAE; a procedure-related colonic infarction occurred in one patient. A minor complication occurred in one patient who developed a groin hematoma. CONCLUSIONS: Superselective embolization may be used for effective, minimally invasive control of acute LGI bleeding.

Norepinephrine-induced hypertension dilates vasospastic basilar artery after subarachnoid haemorrhage in rabbits

BACKGROUND: Vasopressor-induced hypertension is routinely indicated for prevention and treatment of cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH). Mechanisms underlying patients' clinical improvement during vasopressor-induced hypertension remain incompletely understood. The aim of this study was to evaluate angiographic effects of normovolaemic Norepinephrine (NE)-induced hypertension therapy on the rabbit basilar artery (BA) after SAH. METHODS: Cerebral vasospasm was induced using the one-haemorrhage rabbit model; sham-operated animals served as controls. Five days later the animals underwent follow-up angiography prior to and during NE-induced hypertension. Changes in diameter of the BA were digitally calculated in mean microm +/- SEM (standard error of mean). FINDINGS: Significant CVS of 14.2% was documented in the BA of the SAH animals on day 5 compared to the baseline angiogram on day 0 (n = 12, p < 0.01), whereas the BA of the control animals remained statistically unchanged (n = 12, p > 0.05). During systemic administration of NE, mean arterial pressure increased from 70.0 +/- 1.9 mmHg to 136.0 +/- 2.1 mmHg in the SAH group (n = 12, p < 0.001) and from 72.0 +/- 3.1 to 137.8 +/- 1.3 in the control group (n = 12, p < 0.001). On day 5 after SAH, a significant dilatation of the BA in response to norepinephrine could be demonstrated in both groups. The diameter of the BA in the SAH group increased from 640.5 +/- 17.5 microm to 722.5 +/- 23.7 microm (n = 12, p < 0.05; ). In the control group the diameter increased from 716.8 +/- 15.5 microm to 779.9 +/- 24.1 microm (n = 12, p < 0.05). CONCLUSION: This study demonstrated that NE-induced hypertension causes angiographic dilatation of the BA in the SAH rabbit model. Based on these observations, it can be hypothesised that clinical improvement during vasopressor-induced hypertension therapy after SAH might be explained with cerebral vasodilatation mechanisms that lead to improvement of cerebral blood flow.

Decompressive hemicraniectomy in subarachnoid haemorrhage: the influence of infarction, haemorrhage and brain swelling

OBJECTIVE: To analyse decompressive hemicraniectomy (DHC) in patients with aneurysmal subarachnoid haemorrhage (SAH) with regard to infarction, haemorrhage or brain swelling. METHODS: DHC was performed in 43 of 787 patients with SAH. Patients were stratified according to (1) primary brain swelling without and (2) with additional intracerebral haematoma, (3) secondary brain swelling without rebleeding or infarcts and (4) with infarcts or (5) with rebleeding. Outcome was assessed according to the modified Rankin scale at 6 months RESULTS: Overall, 36 of 43 patients (83.7%) with DHC and 241 of 744 patients (32.4%) without DHC have been of a poor grade on admission (World Federation of Neurological Societies grading 4-5; p<0.0001). Favourable outcome was achieved in 11 of 43 (25.6%) patients with DHC. There was no difference in favourable outcome after primary (25%) versus secondary (26.1%) DHC (p = 1.0). Subgroup analysis (brain swelling vs bleeding vs infarcts) revealed no difference in the rate of favourable outcome. In a multivariate analysis, acute hydrocephalus (p = 0.02) and clinical herniation (p = 0.03) were significantly associated with unfavourable outcome. CONCLUSIONS: We conclude that primary and secondary hemicraniectomy may be warranted, irrespective of the underlying aetiology-infarction, haemorrhage or brain swelling. The time from onset of intractable ICP to DHC seems to be crucial, rather than the time from SAH to DHC.