Subarachnoid Hemorrhage and Extracorporeal Blood Purification with HA-380 and High-Volume Hemofiltration: A New Therapeutic Challenge at the Neurocritical Care Unit? A Case Report.

We present the case of a patient with subarachnoid hemorrhage (SAH) secondary to a ruptured cerebral aneurysm and a refractory shock with high doses of vasopressors without a proven source of infection. This patient received therapy with high-volume hemofiltration plus adsorption, resolving the hemodynamic deterioration and with good neurological evolution. Our clinical case proposes that extracorporeal therapies may have a feasibility role in the management of complications of SAH.

Respuesta inmune locorregional y sistémica en hemorragia subaracnoidea aneurismática aguda / Locoregional and systemic immune response in acute aneurysmal subarachnoid hemorrhage

La hemorragia subaracnoidea aneurismática (HSAa) aguda es una enfermedad que afecta a todas las edades, pero fundamentalmente a mujeres jóvenes en torno a los 50 años. Su impacto individual, familiar y sanitario continúa siendo aún inaceptablemente elevado. Esto se debe, en parte, al conocimiento parcial de los mecanismos injuriantes y reparadores que se desencadenan una vez que el aneurisma se rompe y la sangre arterial se vuelca al espacio subaracnoideo y/o ventricular. La respuesta inmune locorregional y sistémica tiene, potencialmente, un rol protagónico como uno de los principales mecanismos en juego desde los primeros minutos (injuria precoz). Su posible rol como puente o enlace hacia la injuria diferida (vasoespasmo-isquemia) también ha sido postulado. La respuesta innata ha recibido mayor atención (investigación) a la fecha. Sin embargo, la respuesta inmune adquirida también ha captado el interés neurocientífico en los últimos años. No menos importante es la interacción neuro-sistémica que caracteriza a esta enfermedad como una entidad clínica con un impacto multiorgánico precoz. En la presente tesis exploramos tanto la respuesta inmune innata como adquirida. Hicimos énfasis en aquellos efectores celulares más importantes y lo complementamos con el análisis de las citoquinas relacionadas y aquellas variables clínicas de interés tales como severidad del sangrado, vasoespasmo, mortalidad y con la técnica seleccionada para el tratamiento del saco aneurismático. Los resultados encontrados son originales, en algunos casos, mientras que otros corroboran hechos ya conocidos, típicos de la enfermedad. Entre los mismos destacamos que la muestra de pacientes enrolados padeció una HSAa aguda grave tanto desde el punto de vista clínico (pobre grado clínico) como tomográfico (abundante sangre volcada al espacio subaracnoideo). En estas condiciones, observamos una hiperleucocitosis con un aumento de los neutrófilos con un mayor estado de activación, particularmente a nivel del LCR. Concomitantemente aumentaron los monocitos totales y sus subpoblaciones a nivel de la sangre periférica. Por otra parte, tanto las células dendríticas como Natural Killers disminuyeron a nivel de la sangre periférica. Particularmente interesante e intrigante resultó ser la objetivación del predominio en LCR de la subpoblación NK CD56brigth CD16-. Con respecto al análisis de los linfocitos y subpoblaciones, observamos un descenso relativo de los mismos a nivel de la sangre periférica, pero no a nivel del LCR. Sin duda alguna, entre los hallazgos originales más atractivos desde un punto de vista patogénico, se encuentran los referentes a las variaciones de las subpoblaciones de células T CD4+ y CD8+ y su mayor estado de activación tanto a nivel de la sangre periférica como del LCR. Pero, además, detectamos un disbalance proinflamatorio del eje Th17/Treg (aumento del cociente) tanto a nivel de la sangre periférica como del LCR. Concomitantemente, la IL-17A aumentó en ambos compartimentos y su incremento a nivel de la sangre periférica en la etapa precoz se asoció al desarrollo ulterior de vasoespasmo y mayor mortalidad. Las restantes citoquinas analizadas (IL-2, IL-4, IL-6, IL-10, TNFα, INFγ) también se incrementaron significativamente tanto a nivel de la sangre periférica como del LCR, pero su incremento no se asoció estadísticamente con ninguna de las variables clínicas de interés mencionadas. Con respecto al posible impacto de la estrategia terapéutica seleccionada para el tratamiento del saco aneurismático sobre la respuesta inmune precoz y diferida, encontramos resultados potencialmente opuestos en las subpoblaciones Th1/Th2 a nivel del LCR, pero sin una asociación estadísticamente significativa con el perfil de citoquinas secretadas a dicho nivel. En suma, hemos demostrado, al igual que diversos investigadores alrededor del mundo, que la respuesta inmune innata tiene un papel protagónico en esta patología. Además, con el estudio del estado de activación hemos jerarquizado el rol de la respuesta inmune adaptativa CD4+ y CD8+. Postulamos al disbalance proinflamatorio del eje Th17/Treg como un potencial jugador patogénico clave y proponemos a la IL-17A como un prometedor biomarcador precoz de mayor morbimortalidad. Sin duda alguna, nuevas estrategias de investigación, experimental y clínica, podrán eventualmente, confirmar nuestros alentadores resultados preliminares comentados

Taurine and aneurysmal subarachnoid hemorrhage prognosis.

Despite its beneficial effects for the cardiovascular system, taurine remains a controversial substance. Taurine increases cardiac muscle strength and prevents arrhythmias, but its benefits go beyond this. Determining taurine levels may become an issue of life or death. In aneurysmal subarachnoid hemorrhage, taurine may be a warning signal informing of the risk of death in a patient. High plasma taurine levels may identify those patients at a high risk for death or a vegetative state at discharge from the hospital; thus, taurine may be a vital marker for the prognosis of this disorder. This is even more relevant considering that the result occurred in patients with a good neurological grade at admission that would usually receive a good prognosis but, despite this, one out of four died or remained in a vegetative state. Maybe taurine is key to explain this apparent paradox.

Hyperchloremia Is Associated With Acute Kidney Injury in Patients With Subarachnoid Hemorrhage.

OBJECTIVE: To assess the prevalence of acute kidney injury in patients with subarachnoid hemorrhage patients. DESIGN: Retrospective analysis of all subarachnoid hemorrhage admissions. SETTINGS: Neurocritical care unit. PATIENTS: All patients with a diagnosis of subarachnoid hemorrhage between 2009 and 2014. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Of 1,267 patients included in this cohort, 16.7% developed acute kidney injury, as defined by Kidney Disease Improving Global Outcome criteria (changes in creatinine only). Compared to patients without acute kidney injury, patients with acute kidney injury had a higher prevalence of diabetes mellitus (21.2% vs 9.8%; p < 0.001) and hypertension (70.3% vs 50.5%; p < 0.001) and presented with higher admission creatinine concentrations (1.21 ± 0.09 vs 0.81 ± 0.01 mg/dL [mean ± SD], respectively; p < 0.001). Patients with acute kidney injury also had higher mean serum chloride and sodium concentrations during their ICU stay (113.4 ± 0.6 vs 107.1 ± 0.2 mmol/L and 143.3 ± 0.4 vs 138.8 ± 0.1 mmol/L, respectively; p < 0.001 for both), but similar chloride exposure. The mortality rate was also significantly higher in patients with acute kidney injury (28.3% vs 6.1% in the non-acute kidney injury group [p < 0.001]). Logistic regression analysis revealed that only male gender (odds ratio, 1.82; 95% CI, 1.28-2.59), hypertension (odds ratio, 1.64; 95% CI, 1.11-2.43), diabetes mellitus (odds ratio, 1.88; 95% CI, 1.19-2.99), abnormal baseline creatinine (odds ratio, 2.48; 95% CI, 1.59-3.88), and increase in mean serum chloride concentration (per 10 mmol/L; odds ratio, 7.39; 95% CI, 3.44-18.23), but not sodium, were associated with development of acute kidney injury. Kidney recovery was noted in 78.8% of the cases. Recovery reduced mortality compared to non-recovering subgroup (18.6% and 64.4%, respectively; p < 0.001). CONCLUSIONS: Critically ill patients with subarachnoid hemorrhage show a strong association between hyperchloremia and acute kidney injury as well as acute kidney injury and mortality.

Protein expression levels in the medullary visceral zone of rats with subarachnoid hemorrhage.

We investigated protein expression in the medullary visceral zone (MVZ) of rats with multiple-organ dysfunction syndrome (MODS) caused by subarachnoid hemorrhage (SAH) to discuss the possible regulatory mechanism of the MVZ in the course of SAH-induced MODS. A SAH-induced MODS model was established in rats by injecting arterial blood into the Willis' circle. Protein expression in the MVZ was analyzed by immunohistochemistry assay. Protein expression in the MVZ peaked 24-36 h after SAH, and was significantly higher than in the control and sham operation groups. Organs at each time point exhibited inflammatory injuries to varying degrees after SAH, which reached a maximum at 24-36 h. Incidences of systemic inflammatory response syndrome and MODS were 100 and 71.67%, respectively, after SAH. There is a consistency between MVZ protein expression and inflammatory changes in each organ after SAH. This prompts the suggestion that the MVZ may be one of the direct regulative centers in SAH-induced MODS, and may be involved in the functional regulation of the surrounding organs after SAH.

C-reactive protein and vasospasm after aneurysmal subarachnoid hemorrhage.

PURPOSE: To evaluate the relationship between C reactive protein levels and clinical and radiological parameters with delayed ischemic neurological deficits and outcome after aneurysmal subarachnoid hemorrhage. METHODS: One hundred adult patients with aneurismal SAH were prospectively evaluated. Besides the baseline characteristics, daily C-reactive protein levels were prospectively measured until day 10 after subarachnoid hemorrhage. The primary end point was outcome assessed by Glasgow Outcome Scale, the secondary was the occurrence of delayed ischemic neurological deficits (DINDs). RESULTS: A progressive increase in the CRP levels from the admission to 3rd postictal day was observed, followed by a slow decrease until the 9th day. Hemodynamic changes in TCD were associated with higher serum CRP levels. Patients with lower GCS scores presented with increased CRP levels. Patients with higher Hunt and Hess grades on admission developed significantly higher CRP serum levels. Patients with higher admission Fisher grades showed increased levels of CRP. A statistically significant inverse correlation was established in our series between CRP serum levels and GOS on discharge and CRP levels. CONCLUSIONS: Higher C-reactive protein serum levels are associated with worse clinical outcome and the occurrence of delayed ischemic neurological deficits. Because C-reactive protein levels were significantly elevated in the early phase, they might be a useful parameter to monitor.

C-reactive protein and vasospasm after aneurysmal subarachnoid hemorrhage1

PURPOSE: To evaluate the relationship between C reactive protein levels and clinical and radiological parameters with delayed ischemic neurological deficits and outcome after aneurysmal subarachnoid hemorrhage. METHODS: One hundred adult patients with aneurismal SAH were prospectively evaluated. Besides the baseline characteristics, daily C-reactive protein levels were prospectively measured until day 10 after subarachnoid hemorrhage. The primary end point was outcome assessed by Glasgow Outcome Scale, the secondary was the occurrence of delayed ischemic neurological deficits (DINDs). RESULTS: A progressive increase in the CRP levels from the admission to 3rd postictal day was observed, followed by a slow decrease until the 9th day. Hemodynamic changes in TCD were associated with higher serum CRP levels. Patients with lower GCS scores presented with increased CRP levels. Patients with higher Hunt and Hess grades on admission developed significantly higher CRP serum levels. Patients with higher admission Fisher grades showed increased levels of CRP. A statistically significant inverse correlation was established in our series between CRP serum levels and GOS on discharge and CRP levels. CONCLUSIONS: Higher C-reactive protein serum levels are associated with worse clinical outcome and the occurrence of delayed ischemic neurological deficits. Because C-reactive protein levels were significantly elevated in the early phase, they might be a useful parameter to monitor. .

Serum C-reactive protein levels predict neurological outcome after aneurysmal subarachnoid hemorrhage.

OBJECTIVES: Our aim was to evaluate the relationship between serum C-reactive protein (CRP) levels and the neurological prognosis and development of vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH). METHODS: Eighty-two adult patients with aSAH diagnoses were prospectively evaluated. Glasgow Coma Scale (GCS) score, Hunt and Hess grade, Fisher grade, cranial CT scans, digital subtraction angiography studies and daily neurological examinations were recorded. Serial serum CRP measurements were obtained daily between admission and the tenth day. Glasgow Outcome Scale (GOS) and the modified Rankin Scale (mRS) were used to assess the prognosis. RESULTS: Serum CRP levels were related to severity of aSAH. Patients with lower GCS scores and higher Hunt and Hess and Fisher grades presented statistically significant higher serum CRP levels. Patients with higher serum CRP levels had a less favorable prognosis. CONCLUSIONS: Increased serum CRP levels were strongly associated with worse clinical prognosis in this study.

Serum C-reactive protein levels predict neurological outcome after aneurysmal subarachnoid hemorrhage / O nível sérico da proteína C-reativa como fator preditivo do prognóstico neurológico após hemorragia subaracnóidea aneurismática

OBJECTIVES: Our aim was to evaluate the relationship between serum C-reactive protein (CRP) levels and the neurological prognosis and development of vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH). METHODS: Eighty-two adult patients with aSAH diagnoses were prospectively evaluated. Glasgow Coma Scale (GCS) score, Hunt and Hess grade, Fisher grade, cranial CT scans, digital subtraction angiography studies and daily neurological examinations were recorded. Serial serum CRP measurements were obtained daily between admission and the tenth day. Glasgow Outcome Scale (GOS) and the modified Rankin Scale (mRS) were used to assess the prognosis. RESULTS: Serum CRP levels were related to severity of aSAH. Patients with lower GCS scores and higher Hunt and Hess and Fisher grades presented statistically significant higher serum CRP levels. Patients with higher serum CRP levels had a less favorable prognosis. CONCLUSIONS: Increased serum CRP levels were strongly associated with worse clinical prognosis in this study.

OBJETIVOS: Nosso propósito foi avaliar a relação entre os níveis séricos de proteína C-reativa (PCR), o prognóstico neurológico e o desenvolvimento de vasoespasmo em pacientes com hemorragia subaracnóidea aneurismática (HSAa). MÉTODOS: Foram avaliados prospectivamente 82 pacientes adultos com diagnóstico de HSAa. Foram anotados em prontuário: a escala de coma de Glasgow (ECG), a escala de Hunt-Hess, a escala de Fisher, TC de crânio, angiografia cerebral e o exame neurológico diário. Foi determinada diariamente a PCR sérica, da admissão ao décimo dia. Foi utilizadas a escala de resultados de Glasgow e a escala de Rankin modificada (mRS) para avaliar o prognóstico. RESULTADOS: Os níveis séricos de PCR estavam relacionados à severidade da HSAa. Pacientes com EGC baixos e altos graus pelas escalas de Hunt-Hess e Fisher tiveram níveis de PCR séricos estatisticamente elevados. Pacientes com altos níveis de PCR séricos tiveram prognóstico menos favorável. CONCLUSÕES: Aumentos dos níveis séricos da PCR foram fortemente associados com pior prognóstico clínico neste estudo.

[Type 2 diabetes mellitus as a prognostic factor in patients with aneurysm clipping after subarachnoid hemorrhage]. / Diabetes mellitus tipo 2 como factor pronóstico en pacientes con clipaje de aneurisma por hemorragia subaracnoidea.

OBJECTIVE: To evaluate if type 2 diabetes mellitus (DM) constitutes a prognostic factor for death and severe disability in patients with aneurysm clipping after subarachnoid hemorrhage (ASH), in an Intensive Care Unit (ICU). MATERIAL AND METHODS: This is a cohort study in patients who were admitted to the ICU between December-2009 and June-2010; 20 with DM (exposed group) and 40 without DM (non-exposed group). Mortality was quantified during ICU stay. At ICU discharge, severe disability was measured through the Glasgow Outcome Scale (category 2); and Glasgow Coma Scale was used to estimate the difference in consciousness level between ICU arrival and discharge. Descriptive statistics and Kaplan Meier survival curves were performed. RESULTS: Mean age was similar between groups (55.8 +/- 11 and 55.6 +/- 15 years, respectively, p = 0.40). A vegetative state was present in one patient without DM. The Glasgow Coma Scale score at ICU entry was 14.1 +/- 1.4 and at discharge, 12.0 +/- 3.6 in the exposed group (p = 0.01); and 13.9 +/- 2.0 us. 13.5 +/- 2.6, in the non-exposed group, respectively (p = 0.45). There were 3 deaths in patients with DM and 5, in patients without DM (p > 0.05); survival time was 12 (95%CI 7, 16) and 10 days (95%CI 7, 13), respectively. Mean glucose remained higher in patients who died at the ICU (p < 0.001). Hydrocephaly was present in 6 exposed patients and 2, non-exposed (p = 0.007). Additionally, 7 and 5 with and without DM, respectively registered a positive blood culture (p = 0.04). CONCLUSIONS: DM was not associated with higher mortality in ICU patients, but hyperglycemia was; thus, it is essential that the intensive care provider watches closely the glycemic control.

Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurysmal subarachnoid hemorrhage.

The goal of the present study was to determine concentrations of E-selectin in both cerebrospinal fluid (CSF) and serum of patients with aneurysmal subarachnoid hemorrhage (SAH) and to evaluate the correlation between the clinical parameters and E-selectin levels. Both CSF and serum samples obtained from 12 patients with aneurysmal SAH and 8 patients with hydrocephalus (control group) without any other known central nervous system disease were assayed for E-selectin by quantitative enzyme-linked immunosorbent assay and the results were compared between the two groups. Mean levels of soluble forms of E-selectin within the first 3 days and on the 5th and 7th days of SAH were 4.0 +/- 7.9, 2.8 +/- 5.2, and 3.1 +/- 4.9 ng/ml in the patient's CSF, and 33.7 +/- 9.2, 35.1 +/- 7.0, and 35.2 +/- 8.7 ng/ml in serum, respectively. In contrast, mean E-selectin levels were 0.1 +/- 0.2 ng/ml in CSF and 8.7 +/- 5.0 ng/ml in serum of control patients. The difference between groups was statistically significant regarding both CSF and serum E-selectin levels (P < 0.05). Thus, we have demonstrated a marked increase of E-selectin concentration in both CSF and serum of patients with aneurysmal SAH compared with control and suggest that blocking the interaction between E-selectin and vascular endothelium may have a beneficial effect on vasospasms.

Endothelin-1 levels in plasma and cerebrospinal fluid of patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

BACKGROUND: Plasma and cerebrospinal fluid (CSF) concentrations of endothelin-1 (ET-1) were measured in patients with subarachnoid hemorrhage (SAH) after aneurysmal rupture and compared with levels of ET-1 in volunteers. We analyze the relationship between levels of ET-1 in both CSF and plasma with the risk of developing cerebral vasospasm (CVS). METHODS: Cerebrospinal fluid and blood samples were collected from 30 selected patients after SAH and from 10 healthy volunteers who were used as control. All samples were stored at -70 degrees C and the levels of ET-1 in CSF and blood were measured by using enzyme-linked immunosorbent assay and Western blot. All patients were submitted to angiography to confirm vasospasm. RESULTS: From the 30 patients admitted at different days of SAH, 18 (60%) developed clinical CVS and 10 (33%) presented angiographic CVS. The levels of ET-1 in the CSF were significantly higher (P = .0001) in patients (1.618 +/- 1.05 fmol/mL) than in controls (0.365 +/- 0.328 fmol/mL). There was statistical difference (P < .05) in CSF levels of ET-1 between each group of the Hunt-Hess scale and controls. The mean plasma concentration of ET-1 was similar (P > .05) in the control group (1.531 +/- 0.753 fmol/mL) and in patients with SAH (1.920 +/- 1.15 fmol/mL). CONCLUSIONS: These findings indicate that a significant rise in ET-1 levels in the CSF, but not in the plasma, occurs in patients who develop CVS after SAH. Our observation suggests that ET-1 might be involved in the pathogenesis of SAH-associated CVS.

Nonthyroidal illness syndrome in patients with subarachnoid hemorrhage due to intracranial aneurysm.

We have previously reported that subarachnoid hemorrhage due to ruptured intracranial aneurysm (SH) is associated with changes in the hormonal profile in the first 24 hours after the event. We proposed that the hormonal changes observed are due to the intense stress to which the patients are exposed. However, the thyroidal hormonal profile is indicative of the presence of a nonthyroidal illness syndrome (NTIS). In this paper, we examined whether the change in the thyroid hormone profile is compatible with a NTIS. Two groups of patients were included in the study: A) 30 patients with SH (21 females and 9 males; 41.7+/-11.4 years) and B) a control group including 25 patients with benign diseases of the spine (BDS) (lumbar disc hernia or stable spinal trauma) (8 females and 17 males; 41.3+/-14.2 years). In a subgroup of eight patients of each group serum triiodothyronine (T3) and reverse T3 levels were measured. The blood samples were obtained between 8:00 and 9:00 AM. The following results were obtained: The SH group had smaller serum T3 and free T4 levels than the BDS group (p<0.05): T3 (ng/mL): SH = 58.7+/-1.1 and BDS = 74.5+/-13.9; free T4 (ng/dL): SH = 0.9+/-0.2 and BDS = 1.1+/-0.3. There was no significant difference in the serum levels of total thyroxine (T4) and thyroid-stimulating hormone (TSH) between the two groups: T4 ( microg/dL): SH = 6.9+/-1.1 and BDS = 7.4+/-2.1; TSH ( microUI/mL): SH = 1.5+/-0.8 and BDS = 1.8+/-1,0. In the sample of eight patients of each group we had the following results: T3 (ng/mL): SH = 66.8+/-3.8 and BDS = 77.2+/-1.1 (p <0.05); reverse T3 (ng/dL): SH = 32.8+/-8 and BDS = 24.7+/-2.2 (NS); T3/ reverse T3 ratio: SH = 2.6+/-0.3 and BDS = 3.3+/-0.4 (NS). Thyreoglobulin and microsomal antibodies were not detectable, except in one patient in the SH group. In conclusion, the SH patients present serum levels of T3 and free T4 significantly lower than that of BDS patients; the thyroidal hormone profile suggests that SH patients have developed the nonthyroidal illness syndrome.

Evaluation of pituitary and thyroid hormones in patients with subarachnoid hemorrhage due to ruptured intracranial aneurysm.

UNLABELLED: It is well known that the central nervous system (CNS) influences the pituitary hormone secretions and that diseases of CNS are frequently associated with an altered endocrine function. The aim of this study has been the evaluation of the serum concentrations of the pituitary and thyroid hormones in a series of patients with subarachnoid hemorrhage due to a ruptured cerebral aneurysm. Thirty-five patients (23 females and 12 males), aged 51.9 +/- 13.3 years on the mean were admitted. They were evaluated to assess the clinical severity of the subarachnoid hemorrhage by Hunt & Hess scale: nine patients were in the grade I, 14 in the grade II, and 12 in the grade III. Blood samples were obtained between 8:00 and 9:00 a.m. and serum hormones were measured by commercial kits (IRMA or MEIA methods). Cortisol serum levels (normal range (NR) = 5 to 18 micro g/dL) were increased in all the patients (mean +/- standard deviation = 31.4 +/- 12.4 micro g/dL). Mean prolactin levels (NR < 20 ng/mL) were 18.6 +/- 17.1 ng/mL and five patients (14.2%) had levels higher than normal. FSH and LH levels were normal according to age and sex: men: FSH = 4 +/- 2.9 mUI/mL (NR = 1 to 10.5 mUI/mL); LH = 6.1 +/- 6.3 mUI/mL (NR = 2 to 12 mUI/mL); premenopausa women: FSH = 2.5 +/- 1.5 mUI/mL (NR = 2.4 to 9.3 mUI/mL); LH 3.9 +/- 5.1 mUI/mL (NR =2 to 15 mUI/mL); post- menopausal women: FSH = 48.3 +/- 18.5 mUI/mL (NR =31 to 134 mUI/mL); LH = 29 +/- 13.8 mUI/mL (NR =16 to 64 mUI/mL). Mean TSH levels were 3.9 +/- 5.2 micro UI/mL (NR =0.5 to 4.7 micro UI/mL) and five patients (14.2%) had levels higher than normal. Mean triiodothyronine levels (T3) were 66.4 +/- 18.7 ng/dL (NR = 45 to 137 ng/dL) and five patients (14.2%) had levels lower than normal (33.8 +/- 9 ng/dL). Mean thyroxine levels (T4) (NR= 4.5 to 12.5 micro g/dL) were 7.4 +/- 1.7 micro g/dL and two patients (5.6%) had levels lower than normal. Thyroglobulin and microsomal antibodies were not detectable. CONCLUSIONS: In the first 24 hours following ictus, the hormonal changes may be due to the stress produced by the intracranial bleeding; thyroid hormone alterations suggest that patients with subarachnoid hemorrhage might have an euthyroid sick syndrome.

Fibrinolytic and factor XIII activity in subarachnoid hemorrhage.

The balance between fibrinolytic activity and coagulation mechanisms seems to play an important role in the rebleeding of a subarachnoid hemorrhage (SAH) due to aneurysmatic rupture. In the present paper we describe our findings in a group of patients (n 10) with SAH. The plasmatic levels of fibrinogen and their degradation products (FDP), APTT, prothrombin activity and factor XIII were determined within 72 hours of initial bleeding or of eventual rebleeding. Factor XIII activity in the first bleeding was 82.1 +/- 4%, while the levels of FDP were 3.8 +/- 1 micrograms/ml. In patients presenting rebleeding (n 4), Factor XIII activity was 67.3 +/- 4.5% the day it manifested, which is significantly less than the values previously observed (p < 0.01), while the FDP level was 4.1 +/- 2 micrograms/ml. The decrease of factor XIII activity suggests an important role as regards clot stability in rupture location. It is also possible to attribute a rebleeding predictive value to its activity reduction.