Electrophysiological assessment of the afferent sensory pathway in cardiac arrest survivors.

BACKGROUND: Hypoxic-ischaemic brain damage in cardiac arrest survivors is global, but postmortem histology could identify parts of the brain that are selectively vulnerable to ischaemia, comprising the thalamus and cortex. We hypothesized that hypoxic-ischaemic brain damage increases along the afferent sensory pathway with a stepwise decrease of detectable somatosensory evoked potential peaks. METHODS: Somatosensory evoked potentials were recorded within 72 h after cardiac arrest in 305 comatose patients after cardiopulmonary resuscitation. We measured the short latency SEP peaks N9, P15, N20, P25 (reflecting the peripheral-thalamo-cortical pathway) and the long latency SEP peaks N35 and N70 (reflecting complex cortico-cortical interactions). Patients with a Cerebral Performance Category score > 2 at 1 year were defined as patients with hypoxic-ischaemic brain damage. RESULTS: Patients with hypoxic-ischaemic brain damage (n = 232) showed a statistically significant decrease of detectable peaks (P < 0.05) along the thalamo-cortical afferent pathway: N13, P15, N20, P25 and N70 peaks were detectable in 99%, 63%, 59%, 55% and 44% patients, respectively. In patients without hypoxic-ischaemic brain damage (n = 73) the N13, P15, N20, P25 peaks were detectable in all, and the N35 and N70 peaks in 98%. Furthermore, in patients with hypoxic-ischaemic brain damage and detectable SEP peaks, P15, N20, P25, N35 and N70, peak latencies were prolonged (P < 0.05) and N20 and N70 amplitudes were decreased (P < 0.05) compared with patients without hypoxic-ischaemic brain damage. CONCLUSION: Extent of hypoxic-ischaemic brain damage in cardiac arrest survivors increases along the afferent sensory pathway, with pronounced vulnerability of thalamic and cortical brain regions.

Influence of hydroxy ethyl starch infusion on serum bilirubin levels in cirrhotic patients treated with artificial liver support.

Serum bilirubin levels are commonly used to assess extracorporeal detoxification by liver support systems. We tested the hypothesis that intravenous colloids administered before liver support treatment could confound bilirubin values. Eight cirrhotic patients received an infusion of a 6% hydroxy ethyl starch solution (10 ml/kg, 30 minutes) before detoxification using a liver support system (FPSA). Bilirubin was measured before and 1 hour after infusion, and after FPSA treatment (7 hours). Infusion of hydroxy ethyl starch was associated with a drop in bilirubin values (mean, 18%, range, 1-44%, p=0.03 versus baseline values). Bilirubin levels were further reduced during FPSA treatment (mean, 27%, range, 22-34%; p=0.02 versus pretreatment values). In conclusion, hydroxy ethyl starch solution may decrease bilirubin levels in hyperbilirubinemic cirrhotic patients receiving extracorporeal detoxification. The role of potentially confounding factors in liver support studies is discussed further.

Effects of sorbent suspension dialysis on plasma amino acid levels in cirrhotic patients with refractory hepatic encephalopathy.

In cirrhotic patients, plasma amino acid levels are severely deranged. A decreased ratio of branched-chain to aromatic amino acids (Fischer ratio) has been implicated in the pathogenesis of hepatic encephalopathy. In this prospective study, we investigated the effects of extracorporeal detoxification on amino acid levels using a sorbent suspension dialysis system. Twenty patients with documented cirrhosis and hepatic encephalopathy grade II-III not responding to standard treatment were randomized to receive either six hours of sorbent dialysis and standardized conventional medical treatment or ongoing medical treatment alone. In contrast to previous uncontrolled studies, no significant effect on amino acid levels, Fischer ratio or clinical grade of hepatic encephalopathy was detected in either treatment group. In conclusion, a 6-hour treatment with sorbent dialysis did not significantly influence plasma levels of amino acids and did not ameliorate the clinical grade of hepatic encephalopathy.

Time-dependency of sensory evoked potentials in comatose cardiac arrest survivors.

OBJECTIVE: To assess the validity of early sensory evoked potential (SEP) recording for reliable outcome prediction in comatose cardiac arrest survivors within 48 h after restoration of spontaneous circulation (ROSC). DESIGN AND SETTING: Prospective cohort study in a medical intensive care unit of a university hospital. PATIENTS: Twenty-five comatose, mechanically ventilated patients following cardiopulmonary resuscitation MEASUREMENTS AND RESULTS: Median nerve short- and long-latency SEP were recorded 4, 12, 24, and 48 h after ROSC. Cortical N20 peak latency and cervicomedullary conduction time decreased (improved) significantly between 4, 12, and 24 h after resuscitation in 22 of the enrolled patients. There was no further change in short-latency SEP at 48 h. The cortical N70 peak was initially detectable in seven patients. The number of patients with increased N70 peak increased to 11 at 12 h and 14 at 24 h; there was no further change at 48 h. Specificity of the N70 peak latency (critical cutoff 130 ms) increased from 0.43 at 4 h to 1.0 at 24 h after ROSC. Sensitivity decreased from 1.0 at 4 h to 0.83 at 24 h after ROSC. CONCLUSION: Within 24 h after ROSC there was a significant improvement in SEP. Therefore we recommend allowing a period of at least 24 h after cardiopulmonary resuscitation for obtaining a reliable prognosis based on SEP.

A controlled study of sorbent suspension dialysis in chronic liver disease and hepatic encephalopathy.

To investigate the role of extracorporeal detoxification in cirrhotic patients with advanced hepatic encephalopathy not responding to medical treatment, 20 patients were randomized to receive six hours of additional sorbent dialysis or ongoing standardized medical treatment. Following treatment, the clinical stage of encephalopathy remained unchanged in both groups. Abnormal sensory evoked potentials improved following sorbent dialysis (N70 latency, 128 ms before versus 110 ms after treatment, P<0,05; cervico-cranial transmission, 7.7 ms versus 6.8 ms, P<0.01) indicating improvement in important aspects of cerebral function. In contrast, brain function remained unchanged following medical treatment (N70 latency, 114 ms versus 113 ms; cervico-cranial transmission, 7.7 ms versus 7.2 ms, P=NS, respectively). Serum benzodiazepine levels decreased significantly after sorbent dialysis but not after medical treatment. Biocompatibility of sorbent dialysis was limited and clinical complications occurred in a proportion of patients. In conclusion, a six-hour treatment with sorbent suspension dialysis did not ameliorate the clinical stage of HE but improved neurophysiologic function in cirrhotic patients who had not responded to conventional medical treatment.

Biocompatibility of a cuprophane charcoal-based detoxification device in cirrhotic patients with hepatic encephalopathy.

Extracorporeal detoxification has been proposed to treat patients with hepatic encephalopathy (HE) not responding to standard therapy. To investigate the biocompatibility of a cuprophane charcoal-based detoxification device, a prospective, randomized, controlled study was performed. Of 41 consecutive patients with cirrhosis and HE grade II or III who did not improve with conventional treatment, 20 patients (median age, 56 years; range, 33 to 71 years; 13 men) were randomly assigned to either ongoing conventional treatment or one additional 6-hour treatment with a sorbent suspension dialysis system. Main outcome parameters were physiological function and blood parameters of biocompatibility. In the 10 patients undergoing combined conventional and sorbent suspension dialysis treatment, blood pressure remained unchanged and body temperature and heart rate increased (P: < 0.01). Platelet count decreased (medians, from 75 to 26 g/L; P: < 0.001) and international normalized ratio increased after combined treatment (2.0 to 2.2; P: < 0.001). Three patients developed bleeding complications during treatment or shortly after. Treated patients showed increases in levels of plasma elastase (104 to 586 microg/L; P: = 0.001), tumor necrosis factor-alpha (5.4 to 7.5 pg/mL; P: = 0.04), and interleukin-6 (118 to 139 pg/mL; P: = 0.04), but not interferon-gamma and E-selectin. No changes were observed in the 10 patients treated conventionally. In conclusion, despite technical refinements compared with charcoal hemoperfusion, biocompatibility of sorbent suspension dialysis is still very limited. Clinical complications were apparently caused by blood-membrane interactions and disseminated intravascular coagulation. We suggest further developments in design and appropriate strategies of anticoagulation to improve the biocompatibility of artificial liver support.

Metabolic encephalopathy in critically ill patients suffering from septic or nonseptic multiple organ failure.

OBJECTIVE: Evaluation of changes in the peak latencies of sensory evoked potentials in different patient groups, to evaluate differences in metabolic encephalopathy of critically ill patients with multiple organ failure as a result of septic or nonseptic conditions. DESIGN: Prospective cohort study. SETTING: Intensive care units of the university hospital, Vienna. PATIENTS: Patients (n = 103) treated on an intensive care unit because of multiple organ failure with additional metabolic encephalopathy. Multiple organ failure was induced by sepsis (group A; n = 56), surgery (group B; n = 29), or both (group C; n = 18). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Metabolic encephalopathy was determined by measuring median nerve-stimulated short-latency and long-latency sensory evoked potentials. No differences in the peak latencies of the sensory evoked potentials were detected among the groups. Septic patients had a N70 peak latency of 131+/-21 msecs, nonseptic postsurgical patients of 132+/-17 msecs, and septic postsurgical patients of 134+/-17 msecs. The cervicomedullary N13 to cortical N20 conduction times were 6.4+/-1 msec, 6.4+/-1.4 msecs, and 6.8+/-1.2 msecs, respectively. All measured peak latencies were significantly prolonged compared with peak latencies of healthy controls. The severity of illness assessed by the Acute Physiology and Chronic Health Evaluation III score was not different between the three groups. An increase of the delay of N70 peak latencies was significantly correlated with the severity of illness (r2 = .15; p < .00005). CONCLUSION: There was no difference in sensory evoked potential measurements detectable among septic patients with multiple organ failure, nonseptic postsurgical patients with multiple organ failure, and septic postsurgical patients with multiple organ failure. The N70 peak latency was significantly correlated with the severity of illness but not with the presence or absence of sepsis. In postsurgical patients with multiple organ failure and superimposed sepsis, the N70 peak latencies were not further prolonged compared with postsurgical patients without sepsis.

Bladder volume determination: portable 3-D versus stationary 2-D ultrasound device.

OBJECTIVE: To investigate how accurately a portable three-dimensional (3-D) scanner and a multipurpose two-dimensional (2-D) real-time scanner determined bladder volumes. STUDY DESIGN: Prospective, controlled clinical trial, single-blind, crossover design. SETTING AND PARTICIPANTS: Twenty-three inpatients with permanent bladder catheters participated voluntarily in this study. METHODS: The bladders of 20 patients were filled through an indwelling catheter with 60, 110, 160, 210, and 260 mL sterile normal saline. Volumes were measured twice with each device. Measurements were compared with the actual bladder volumes. RESULTS: The 2-D device showed better reproducibility, particularly at lower bladder volumes. The 3-D scanner showed a significant difference between the two measurements at 160 mL (p<.05) and had poor reproducibility at 110, 210, and 260 mL. Both devices overestimated actual bladder volume at fillings of <160 mL and underestimated it at fillings of > or =160 mL. The range between the 25th and 75th percentiles was always larger for the 3-D scanner, except for the 210 mL reading. CONCLUSION: Both devices showed sufficient accuracy for clinical practice. Ultrasound measurements of >110 mL should be followed by catheterization to detect potentially harmful bladder volumes.

Improved outcome prediction in unconscious cardiac arrest survivors with sensory evoked potentials compared with clinical assessment.

OBJECTIVE: To compare the prognostic ability of sensory evoked potentials in cardiac arrest survivors with the outcome predicted by a panel of experienced emergency physicians based on detailed prehospital, clinical, and laboratory data. DESIGN: Inception cohort study. SETTING: Medical intensive care unit and department of emergency medicine at a university hospital. PATIENTS: A total of 162 unconscious, mechanically ventilated patients who survived > or =24 hrs after resuscitation from cardiac arrest. INTERVENTIONS: Recording of sensory evoked potentials and outcome prediction after review of detailed clinical and laboratory data by emergency physicians within 24 hrs after cardiac arrest. MEASUREMENTS AND MAIN RESULTS: At 6 months, the outcome of 36 patients was classified as favorable and 126 patients were rated as poor. After review of prehospital data, emergency physicians predicted favorable vs. poor outcome with a sensitivity of 70% and a specificity of 65%. After additional assessment of data 1 hr after cardiac arrest, the sensitivity of emergency physician predictions increased to 80%, whereas the specificity decreased to 48%. Outcome prediction by emergency physicians was most accurate after obtaining detailed patient data 24 hrs after cardiac arrest (sensitivity, 81%; specificity, 58%). In 35 of 36 patients with favorable outcomes, the cortical evoked potential N70 peak was detected between 72 and 128 msec. Of 113 patients with an N70 peak latency >130 msec or an absent N70 peak, all except one had a poor outcome. By using a cutoff of 130 msec, the N70 peak latency alone had a sensitivity of 94% and a specificity of 97%. The predictive accuracy of the N70 peak latency was significantly higher than the clinical assessment 24 hrs after cardiac arrest (91% vs. 76%, p = .0003). CONCLUSION: In unconscious cardiac arrest survivors, a recording of long-latency sensory evoked potentials is more accurate in predicting individual outcome than an emergency physician review of clinical data.

Partial pressure of ammonia versus ammonia in hepatic encephalopathy.

Ammonia is considered the major pathogenetic factor of cerebral dysfunction in hepatic failure. The correlation between total plasma ammonia and the severity of hepatic encephalopathy (HE), however, is variable. Because ammonia that is present in gaseous form readily enters the brain, the correlation with the grade of HE of the pH-dependent partial pressure of gaseous ammonia (pNH(3)) could be better than that of total arterial ammonia levels. To test this hypothesis, 56 cirrhotic patients with acute episodes of clinical HE (median age, 54 years; range, 21-75) were studied by clinical examination and by long-latency median-nerve sensory-evoked potentials (SEPs) N70 peak, an objective and sensitive electrophysiological measure of HE. pNH(3) was calculated from arterial blood according to published methods. The clinical grade of HE correlated (P <.001) with both pNH(3) and total ammonia, but correlation was stronger with pNH(3) (r =.79 vs.69, P =.01). A similar correlation was found for N70 peak latency (r =.71 with pNH(3) vs.64 with total ammonia, respectively, P =.08). In summary, arterial pNH(3) correlates more closely than total ammonia with the degree of clinical and electrophysiological abnormalities in HE. These findings support the ammonia hypothesis of HE and suggest that pNH(3) might be superior to total ammonia in the pathophysiological evaluation of HE.

Heavy chronic alcohol abuse has no additional adverse effect on the function of extrahepatic organs and ICU mortality in patients with liver cirrhosis.

BACKGROUND AND AIMS: We questioned whether heavy chronic alcohol abuse influences extrahepatic organ failure and ICU mortality in cirrhotic patients admitted to a medical intensive care unit. PATIENTS AND METHODS: Medical records of 208 consecutive cirrhotic critically ill patients were reviewed. Patients were classified into two groups. Group A comprised 144 patients with liver cirrhosis due to heavy chronic alcohol abuse and group B, 64 patients with liver cirrhosis due to non-alcoholic causes. The presence of extrahepatic organ failures in patients of both groups was assessed with parameters determined on the day of admission to the ICU. Furthermore, ICU mortality was determined. RESULTS: The occurrence of extrahepatic organ failure was similar in group A and group B (83% vs. 80%; p = NS). The rate of extrahepatic organ failure was 1.7 +/- 1.2 organs in group A, compared to 1.4 +/- 1 organs in group B (p = NS). ICU mortality was 53% in group A and 44% in group B (p = NS). An increase in the number of extrahepatic organ failures was associated with a concomitant increase in ICU mortality in both groups of patients. CONCLUSION: The occurrence of extrahepatic organ failure and ICU mortality was not different between patients with liver cirrhosis secondary to heavy chronic alcohol abuse and patients with liver cirrhosis due to nonalcoholic causes. Cirrhotic patients should be admitted to a medical intensive care unit for extended intensive care treatment prior to the occurrence of extrahepatic multiple organ failure, independent of the underlying aetiology.

Fulminant lethal tuberculous pneumonia (Sepsis tuberculosis gravissima) with ARDS in a non-immunocompromised western European middle-aged man.

We report the case of a 42 years old, non-immunocompromised native Austrian living in Vienna. He presented at home with severe dyspnea and had to be intubated immediately. Shortly after hospital admission, he developed severe adult respiratory distress syndrome (ARDS) and septic shock with massive, bilobar patchy to confluent infiltrations and a need for norepinephrine. A CT-scan revealed severe loss of functional lung tissue with areas of consolidation and multiple communicating cystic spaces. Air leaking into the mediastinum through fistulas produced pneumomediastinum, pneumoperitoneum, and a massive soft tissue emphysema. Bronchoalveolar lavage performed within the first 24 hours of admission revealed + of acid-fast bacilli. Even though appropriate tuberculostatic medication was started immediately, the patient succumbed the next day to ARDS due to massive tuberculous pneumonia and miliary disease (Sepsis tuberculosis gravissima).