Catherine Ract

Critically ill old and the oldest-old patients in intensive care: short- and long-term outcomes

ObjectiveThe purpose of this study was to examine characteristics and outcome of the old, very old and oldest-old ICU patientsDesignThis is a cohort study.SettingThe study was set in a ten-bed medical ICU in a university hospital.ParticipantsThere were 410 patients classified in three subgroups: old, 75–79 years (n=184; 44.4%), very old, 80–84 (n=137, 33.4%) and the oldest-old, ≥85 (n=91; 22.2%).MeasurementsUnderlying medical conditions, organ dysfunction, severity of illness, length of stay, use of mechanical ventilation, therapeutic activity and nosocomial infections were recorded. Multivariate analysis was conducted to identify risk factors for ICU and long-term mortality.ResultsCharacteristics at ICU admission did not differ among the three groups. ICU length of stay, therapeutic activity, mechanical ventilation and nosocomial infection(s) decreased with age. ICU survival rates for those below 75, 75–79, 80–84 and over 85 years were 80, 68, 75 and 69%, respectively; survival rates at 3 months were 54, 56 and 51%, respectively. APACHE II score [odds ratio (OR): 1.11] was identified as the only factor associated with ICU mortality, and age (OR: 2.17, for patients ≥85 years old and 1.82, for patients 80–84 years old) and limitation of activity before admission (OR: 1.74) as factors associated with long-term mortality.ConclusionIn a population of patients ≥75 years old, very old age is not directly associated with ICU mortality. After ICU discharge, deaths occurred predominantly during the first 3 months: age and prior limitation of activity were associated with the risk of dying.

Diagnosis and follow-up of infections in intensive care patients: value of C-reactive protein compared with other clinical and biological variables.

OBJECTIVE To evaluate diagnostic and prognostic values of C-reactive protein (CRP) dosage in critically ill patients. DESIGN Prospective, observational study. SETTING Medical intensive care unit (ICU) in a university hospital. PATIENTS A consecutive series of 74 patients admitted to the ICU. INTERVENTION CRP measurements at admission and every 4 days thereafter. MEASUREMENTS AND MAIN RESULTS At admission, 28 patients (38%) had microbiologically proven infections. Compared with uninfected patients, their mean +/- SD CRP level was 191 +/- 123 vs. 83 +/- 91 mg/L (p < .0001), respectively, white blood cell count was 15.3 +/- 7.5 vs. 11.4 +/- 5.3 G/L (p = .01), and the systemic inflammatory response syndrome (SIRS) was present for 96% vs. 67% (p = .008). No threshold value could be identified to discriminate between these two populations. Multivariate analysis retained CRP and SIRS as the only variables independently associated with the presence of an infection. The combination of CRP > or = 50 mg/L with SIRS was identified as the best model to diagnose infection at admission. This multivariate model performed better than temperature, CRP alone, and white blood cell count. Among the 28 infected patients, 10 recovered; CRP values decreased significantly in this population as compared with patients with persistent infection (-130 +/- 110 vs. 12 +/- 97 mg/L, respectively; p = .004). A CRP decrease > or = 50 mg/L between admission and day 4 was the best cutoff value to diagnose recovery (sensitivity 89%, specificity 79%). CONCLUSION CRP in combination with SIRS was useful to diagnose infection in ICU patients; a CRP decrease > or = 50 mg/L between admission and day 4 was the best predictor of recovery.

Relationship between intracranial pressure, mild hypothermia and temperature-corrected PaCO2 in patients with traumatic brain injury.

Objective: To study the effects of mild hypothermia and associated changes in temperature-corrected PaCO2 (cPaCO2) on intracranial pressure (ICP), mean velocity of the middle cerebral artery (Vm), and venous jugular saturation in O2 (SjvO2) in patients with severe traumatic brain injury (TBI).¶Design: Prospective, observational study.¶Setting: Intensive care unit.¶Patients: Severe TBI patients mechanically ventilated, sedated and paralyzed.¶Interventions: Twenty patients were subjected to four consecutive periods: (a) normocapnia-normothermia; (b) hypocapnia-normothermia, where hypocapnia was induced by an increase in minute volume; (c) hypocapnia-hypothermia, where hypocapnia was induced by hypothermia maintaining the ventilatory settings constant; (d) normocapnia-hypothermia, where normocapnia was achieved by a decrease in minute volume.¶Measurements and results: cPaCO2 was 41 ± 8 mmHg in periods 1 and 4, and 31 ± 7 mmHg in periods 2 and 3. Core temperature was 37.1 ± 0.8 °C in periods 1 and 2, and 34.1 ± 1.1 °C in periods 3 and 4. End-tidal CO2 and cPaCO2 values showed no difference between periods 1 and 4 and periods 2 and 3. ICP and Vm were dependent on cPaCO2 but independent of core temperature values. SjvO2 was related to cPaCO2 and was significantly higher during period 3 than during period 2 (P < 0.05).¶Conclusion: The decrease in ICP was similar when hypocapnia was induced by hyperventilation or as a result of hypothermia alone. The relationship between cPaCO2 and ICP might predict variations in ICP during changes in core temperature. Further studies are needed to confirm the cerebral metabolic effects of moderate hypothermia in TBI patients.

Early SjvO2 monitoring in patients with severe brain trauma.

Objective: To investigate early cerebral variables after minimal resuscitation and to compare the adequacy of a cerebral perfusion pressure (CPP) guideline above 70 mmHg, with jugular bulb venous oxygen saturation (SjvO2) monitoring in a patient with traumatic brain injury (TBI). Design: Prospective, observational study. Setting: Anesthesiological intensive care unit. Patients: 27 TBI patients with a postresuscitation Glasgow Coma Scale score less than 8. Intervention: After initial resuscitation, cerebral monitoring was performed and CPP increased to 70 mmHg by an increase in mean arterial pressure (MAP) with volume expansion and vasopressors as needed. Measurements and results: MAP, intracranial pressure (ICP), CPP, and simultaneous arterial and venous blood gases were measured at baseline and after treatment. Before treatment, 37 % of patients had an SjvO2 below 55 %, and SjvO2 was significantly correlated with CPP (r = 0.73, p < 0.0001). After treatment, we observed a significant increase (p < 0,0001) in CPP (78 ± 10 vs 53 ± 15 mmHg), MAP (103 ± 10 vs 79 ± 9 mmHg) and SvjO2 (72 ± 7 vs 56 ± 12), without a significant change in ICP (25 ± 14 vs 25 ± 11 mmHg). Conclusion: The present study shows that early cerebral monitoring with SjvO2 is critical to assess cerebral ischemic risk and that MAP monitoring alone is not sensitive enough to determine the state of oxygenation of the brain. SjvO2 monitoring permits the early identification of patients with low CPP and high risk of cerebral ischemia. In emergency situations it can be used alone when ICP monitoring is contraindicated or not readily available. However, ICP monitoring gives complementary information necessary to adapt treatment.

Endothelial oxidative stress induced by serum from patients with severe trauma hemorrhage

ObjectiveShock induces oxidative stress by ischemia-reperfusion phenomenon. Endothelial cells are involved in the inflammatory response and oxidative stress responsible for microcirculation impairment and organ failure. We examined the potential of serum from patients to induce in vitro reactive oxygen species production by cultured human umbilical vein endothelial cells (HUVECs).PatientsThree groups were compared: hemorrhagic shock trauma patients, isolated brain injured patients, and healthy volunteers.MethodsIn the hemorrhagic shock group we sought a correlation between reactive oxygen species production and severity of shock. Serum was separated and perfused in an in vitro model of perfused HUVECs. Ex vivo reactive oxygen species production was assessed by fluorescence microscopy using dichlorodihydrofluorescein, an intracellular dye oxidized by H2O2. Results are expressed in proportional change from baseline and normalized by protidemia to control for variation related to hemodilution.ResultsReactive oxygen species production by endothelial cells exposed to serum from hemorrhagic shock patients (46.2±24.9%) was significantly greater than in those with brain injury (3.9±35.1%) and in healthy volunteers (−6.8±5.8%). In the hemorrhagic shock group dichlorodihydrofluorescein fluorescence was strongly correlated positively to Simplified Acute Physiology Score II and lactatemia and negatively to [HCO3−].ConclusionsSerum from trauma patients with hemorrhagic shock induces reactive oxygen species formation in naive endothelial cells which is correlated to shock severity.

Comparison of dopamine and norepinephrine after traumatic brain injury and hypoxic-hypotensive insult

After severe brain trauma, blood-brain barrier disruption and alteration of cerebral arteriolar vasoreactive properties may modify the cerebral response to catecholamines. Therefore, the goal of the present study was to compare the effects of dopamine and norepinephrine in a model of brain injury that consisted of a weight-drop model of injury complicated by a 15-min hypoxic-hypotensive insult (HH). Sprague-Dawley rats (n = 7 in each group) received, after brain injury, an infusion of either norepinephrine (TNE group) or dopamine (TDA group) in order to increase cerebral perfusion pressure (CPP) above 70 mm Hg. In addition, a control group (C group, no trauma) and a trauma group (T group, brain injury, no catecholamine infusion) were studied. Mean arterial pressure (MAP), intracranial pressure (ICP, intraparenchymal fiberoptic device), and local cerebral blood flow (LCBF, extradural laser-Doppler fiber) were measured throughout the protocol. In T group, brain injury and HH induced a decrease in CPP (by an increase of ICP and a decrease of MAP), and a decrease of LCBF. Both norepinephrine and dopamine failed to increase CPP, and ICP was significantly higher in TNE and TDA groups than in T group. Interestingly, norepinephrine was not able to alleviate the decrease in MAP. Neither norepinephrine or dopamine could induce an increase of MAP. LCBF decreased similarly in T, TNE and TDA groups. In conclusion, norepinephrine and dopamine are not able to restore values of CPP above 70 mm Hg in a model of severe brain trauma. Furthermore, their systemic vasopressor properties are altered.

Hypoxia-hypotension decreases pressor responsiveness to exogenous catecholamines after severe traumatic brain injury in rats

ObjectiveTo quantify the phenylephrine pressor responsiveness after severe brain injury combined with hypoxia-hypotension, and to study the respective roles of brain injury and hypoxia-hypotension in the observed alteration. DesignRandomized study. SettingAccredited animal laboratory. SubjectsAdult Sprague Dawley rats. InterventionsAnesthetized animals were assigned to control, brain injury, hypoxia-hypotension, and brain injury combined with hypoxia-hypotension groups. Brain injury was induced with an impact-acceleration device. During the 15-min hypoxia-hypotension, arterial oxygen pressure was decreased to 40 torr (5.3 kPa) and mean arterial pressure to 30 mm Hg. Thirty-six of the 53 included rats were alive at the end of hypoxia-hypotension (nine animals per group). In an additional group (Hypo, n = 8), mean arterial pressure was lowered to the level observed in brain injury combined with hypoxia-hypotension with pentobarbital infusion. Sixty minutes after injuries (T60), animals received 0.1, 1, and 10 &mgr;g/kg phenylephrine in a random order. Pressor responsiveness to phenylephrine was defined as maximal postinjection minus preinjection mean arterial pressure. Measurements and Main Results During hypoxia-hypotension, mortality was higher and residual restored blood volume was lower (p < .01) in the animals with brain injury and hypoxia-hypotension compared with hypoxia-hypotension alone. At T60, mean arterial pressure (mm Hg) was lower (p < .01) in the brain injury group (83 ± 22) compared with controls (110 ± 10) and in brain injury combined with hypoxia-hypotension (76 ± 18) compared with controls and hypoxia-hypotension (107 ± 14). Pressor responsiveness (mm Hg) to 1 and 10 &mgr;g/kg phenylephrine was less (p < .05) in brain injury combined with hypoxia-hypotension (15 ± 6 and 44 ± 8) and hypoxia-hypotension (15 ± 3 and 44 ± 8) compared with controls (26 ± 2 and 57 ± 11). No significant difference was observed for phenylephrine pressor responsiveness between controls and the Hypo group (25 ± 5 and 66 ± 7). ConclusionsCombination of brain injury and hypoxia-hypotension induces a severe hemodynamic alteration associated with a decreased pressor responsiveness to phenylephrine. Transient hypoxia-hypotension is responsible for the depressed &agr;-1 adrenergic reactivity.

The Limits of Succinylcholine for Critically Ill Patients

BACKGROUND:Urgent tracheal intubations are common in intensive care units (ICU), and succinylcholine is one of the first-line neuromuscular blocking drugs used in these situations. Critically ill patients could be at high risk of hyperkalemia after receiving succinylcholine because one or more etiologic factors of nicotinic receptor upregulation can be present, but there are few data on its real risk. Our objectives in this study were to determine the factors associated with arterial potassium increase (&Dgr;K) and to assess the occurrence of acute hyperkalemia ≥6.5 mmol/L after succinylcholine injection for intubation in the ICU. METHODS:In a prospective, observational study, all critically ill patients intubated with succinylcholine in an ICU were screened. Only intubations with arterial blood gases and potassium measurements before and after (Kafter) a succinylcholine injection were studied. RESULTS:During 18 months, 131 critically ill patients were intubated after receiving succinylcholine with arterial potassium before and after intubation (Kafter) for a total of 153 intubations. After multivariate analysis, the only factor associated with &Dgr;K was the length of ICU stay before intubation (&rgr; = 0.561, P < 0.001). The factors associated with Kafter ≥6.5 mmol/L (n = 11) were the length of ICU stay (P < 0.001) and the presence of acute cerebral pathology (P = 0.047). The threshold of 16 days was found highly predictive of acute hyperkalemia ≥6.5 with 37% (95% confidence interval: 19%–58%) of Kafter ≥6.5 after the 16th day compared with only 1% (95% confidence interval: 0%–4%) of Kafter ≥6.5 when succinylcholine was injected during the first 16 days. CONCLUSIONS:This study shows that the risk of &Dgr;K after succinylcholine injection is strongly associated with the length of ICU stay. The risk of acute hyperkalemia ≥6.5 mmol/L is highly significant after 16 days.

Heparin-induced thrombocytopenia: Successful biological and clinical management with lepirudin despite severe renal impairment

Heparin-induced thrombocytopenia: Successful biological and clinical management with lepirudin despite severe renal impairment -

Sudden Loss of Consciousness during a Flight

despite 3 of them having received hyperbaric oxygen therapy. Only 2 patients completely recovered, included 1 treated by hyperbaric oxygen therapy at 48 h, good prognosis being probably related more to the limited extent of the cerebral lesions than to late hyperbaric oxygen therapy [2] . Despite its rarity, medical teams involved in the management of strokes should be aware of this aetiology, in order to rapidly consider this diagnosis in a patient with sudden onset of a neurological deficit or coma during a flight. Indeed, the initial CT abnorBronchogenic cysts can very rarely be responsible for air embolism in a context of significantly increased atmospheric pressure. To our knowledge, only 7 similar cases have been reported in the Medline literature [1] . This cause of stroke can be quickly diagnosed in a suggestive context and if brain imaging (including CT scanner) is properly interpreted. We herewith describe a patient who suddenly became comatose during a flight, due to diffuse cerebral ischaemia caused by air embolism from a pulmonary bronchogenic cyst and review the previous literature.