Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs.

We previously found mild hypothermia (34-36 degrees C), induced before cardiac arrest, to improve neurologic outcome. In this study we used a reproducible dog model to evaluate mild hypothermia by head cooling during arrest, continued with systemic cooling (34 degrees C) during recirculation and for 1 h after arrest. In four groups of dogs, ventricular fibrillation (no flow) of 12.5 min at 37.5 degrees C was reversed with cardiopulmonary bypass and defibrillation in less than or equal to 5 min, and followed by controlled ventilation to 20 h and intensive care to 96 h. In Study A we resuscitated with normotension and normal hematocrit; Control Group A-I (n = 12) was maintained normothermic, while Treatment Group A-II (n = 10) was treated with hypothermia. In Study B we resuscitated with hypertension and hemodilution. Control Group B-I (n = 12) was maintained normothermic (6 of 12 were not hemodiluted), while Treatment Group B-II (n = 10) was treated with hypothermia. Best overall performance categories (OPCs) achieved between 24 and 96 h postarrest were in Group A-I: OPC 1 (normal) in 0 of 12 dogs, OPC 2 (moderate disability) in 2, OPC 3 (severe disability) in 7, and OPC 4 (coma) in 3 dogs. In Group A-II, OPC 1 was achieved in 5 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.001), OPC 3 in 1, and OPC 4 in 0 dogs. In Group B-I, OPC 1 was achieved in 0 of 12 dogs, OPC 2 in 6, OPC 3 in 5, and OPC 4 in 1 dog. In Group B-II, OPC 1 was achieved in 6 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.05), and OPC 3 or 4 in 0 dogs. Mean neurologic deficit and brain histopathologic damage scores showed similar significant group differences. Morphologic myocardial damage scores were the same in all four groups. We conclude that mild brain cooling during and after insult improves neurologic outcome after cardiac arrest.

Thrombosis of superior vena cava during total parenteral nutrition, managed successfully with low dose streptokinase.

Superior vena cava syndrome due to catheter related thrombosis, developed in a patient receiving total parenteral nutrition. Local infusion of low dose streptokinase immediately proximal to the thrombus, was strikingly successful and may be the treatment of choice for this condition.

Cerebral and systemic arteriovenous oxygen monitoring after cardiac arrest. Inadequate cerebral oxygen delivery.

BACKGROUND: After prolonged cardiac arrest, under controlled normotension, cardiac output and cerebral blood flow are reduced for several hours. This dog study documents for the first time the postarrest reduction in oxygen (O2) delivery in relation to O2 uptake for brain and entire organism. METHODS: In eight dogs we used our model of ventricular fibrillation (VF) cardiac arrest of 12.5 min, reperfusion with brief cardiopulmonary bypass, and controlled normotension, normoxemia, and mild hypocapnia to 24 h. RESULTS: Between 4 and 24 h after cardiac arrest, cardiac output decreased by about 25% and the systemic arteriovenous O2 content difference doubled, while the calculated systemic O2 utilization coefficient (O2 UC) increased and the systemic venous PO2 decreased, both not to critical levels. The cerebral arteriovenous O2 content difference however, which was 5.6 +/- 1.7 ml/dl before arrest, increased between 1 and 18 h, to 10.8 +/- 3.2 ml/dl at 4 h. The cerebral O2 UC increased and the cerebral venous PO2 decreased, both to critical levels. CONCLUSIONS: After prolonged cardiac arrest in dogs with previously fit hearts, the reduction of O2 transport to the brain is worse than its reduction to the whole organism. Monitoring these values might help in titrating life-support therapies.

Detoxification with hemabsorption after cardiac arrest does not improve neurologic recovery. Review and outcome study in dogs.

We and others hypothesized that noxious substances released after prolonged cardiac arrest from malfunctioning liver, kidneys, or intestine (e.g. bacterial toxins, aromatic amino acids), might hamper recovery of the brain. The highly detoxifying effect of hemabsorption (i.e. hemoperfusion) with microencapsulated activated carbon has been demonstrated in other diseases. We used our dog model of ventricular fibrillation cardiac arrest of 15 min (n = 2 x 4) or 12.5 min (n = 2 x 6), reversed by brief (high flow) cardiopulmonary bypass (CPB). In half of the dogs in each insult group, a charcoal filter (HemoKart) was inserted into the circuit of CPB at low flow, from start of reperfusion to 4 h. Intermittent positive pressure ventilation was to 20 h and intensive care to 96 h after cardiac arrest. Bacterial blood cultures were positive in most of the dogs in both groups 30 min to 20 h after cardiac arrest (but not later) and were uninfluenced by hemabsorption. In the control groups to 4 h after cardiac arrest, serum levels of potentially injurious aromatic amino acids (e.g. phenylalanine, tyrosine) and of branched-chain/aromatic amino acid ratios, remained unchanged. From 12 to 48 h after cardiac arrest, aromatic amino acid levels increased (worsened). The branched-chain/aromatic amino acid ratios changed accordingly in the opposite direction. In the hemabsorption groups to 4 h after cardiac arrest, all amino acid levels were reduced, aromatic amino acids more so than branched-chain amino acids, thus increasing (improving) the ratio, compared with controls (P < 0.01). There was no group difference after discontinuance of hemabsorption at 4 h. Outcome in terms of overall performance categories and neurologic deficit scores from 24 to 96 h and brain histopathologic damage scores 96 h after cardiac arrest, were not significantly different between groups. The lack of a beneficial outcome effect of hemabsorption to 4 h after cardiac arrest does not support the self-intoxication hypothesis. The amino acid levels later after cardiac arrest suggest that more prolonged hemabsorption and more encompassing detoxification treatments, such as plasma phoresis or total body blood washout, might be evaluated.

Mild hypothermia after cardiac arrest in dogs does not affect postarrest cerebral oxygen uptake/delivery mismatching.

PURPOSE: To compare measurements of cerebral arteriovenous oxygen content differences (oxygen extraction ratios, oxygen utilization coefficients) in dogs after cardiac arrest, resuscitated under normothermia vs. mild hypothermia for 1-2 h or 12 h. METHODS: In 20 dogs, we used our model of ventricular fibrillation (no blood flow) of 12.5 min, reperfusion with brief cardiopulmonary bypass, and controlled ventilation, normotension, normoxemia, and mild hypocapnia to 24 h. We compared a normothermic control Group I (37.5 degrees C) (n = 8); with brief mild hypothermia in Group II (core and tympanic membrane temperature about 34 degrees C during the first hour after arrest) (n = 6); and with prolonged mild hypothermia in Group III (34 degrees C during the first 12 h after arrest) (n = 6). RESULTS: In Group I, the cerebral arteriovenous O2 content difference was 5.6 +/- 1.6 ml/dl before arrest; was low during reperfusion (transient hyperemia) and increased (worsened) significantly to 8.8 +/- 2.8 ml/dl at 1 h, remained increased until 18 h, and returned to baseline levels at 24 h after reperfusion. These values were not significantly different in hypothermic Groups II and III. The cerebral venous (saggital sinus) PO2 (PssO2) was about 40 mmHg (range 29-53) in all three groups before arrest and decreased significantly below baseline values, between 1 h and 18 h after arrest; the lowest mean values were 19 +/- 19 mmHg in Group I, 15 +/- 8 in Group II (NS), and 21 +/- 3 in Group III (NS). Postarrest PssO2 values of < or = 20 mmHg were found in 6/8 dogs in Group I, 5/6 in Group II and 4/6 in Group III. Among the 120 values of PssO2 measured between 1 h and 18 h after arrest, 32 were below the critical value of 20 mmHg. CONCLUSIONS: After prolonged cardiac arrest, critically low cerebral venous O2 values suggest inadequate cerebral O2 delivery. Brief or prolonged mild hypothermia after arrest does not mitigate the postarrest cerebral O2 uptake/delivery mismatching.

Multifocal cerebral blood flow by Xe-CT and global cerebral metabolism after prolonged cardiac arrest in dogs. Reperfusion with open-chest CPR or cardiopulmonary bypass.

Using the stable xenon-enhanced computed tomography (Xe-CT) method in dogs, we studied local, regional and global cerebral blood flow (LCBF, rCBF and gCBF) in two sham experiments and nine cardiac arrest experiments. Within the same experiments without arrest, gCBF and rCBF values were reproducible and stable. LCBF values varied over time. In group I (n = 4), ventricular fibrillation cardiac arrest (no blood flow) of 10 min was reversed by open-chest cardiopulmonary resuscitation (CPR). In group II (n = 5), ventricular fibrillation cardiac arrest of 12.5 min was reversed by brief closed-chest cardiopulmonary bypass. This was followed by controlled ventilation, normotension, normoxia, normocarbia and normothermia to 4 h (n = 7) or 20 h (n = 2) postarrest. The postarrest CBF patterns were similar in both groups. Open-chest CPR during ventricular fibrillation generated near-baseline gCBF and lower LCBF ranges. During postarrest spontaneous circulation, transient diffuse hyperemia was without low-flow regions, longer in brain stem and basal ganglia than in neocortex. During delayed hypoperfusion at 1-4 h postarrest (n = 9), mean gCBF was 44-60% baseline, rCBF in primarily gray matter regions was 15-49 ml/100 cm3 per min and LCBF voxels with trickle-flow and low-flow values, in percent of CT cut area, were increased over baseline. Global CMRO2 (n = 3 of group II) recovered to near baseline values between 1 and 4 h postarrest, while gCBF and O2 delivery were about 50% baseline (mismatching of O2 uptake and O2 delivery).

Type II diabetes mellitus, congestive heart failure, and zinc metabolism.

Zinc status was assessed in patients with type II diabetes mellitus and congestive heart failure (CHF). Three groups of patients were enrolled into the study: Group 1: 15 patients with type II diabetes mellitus and CHF; Group 2: 20 patients with isolated type II diabetes mellitus; and Group 3: nine patients with isolated CHF. Twenty-four-hour urine was measured for creatinine, protein, and zinc, and blood was drawn for creatinine, proteins, liver enzymes, hemoglobin A1c, and zinc. Insulin treatment and hemoglobin A1c were comparable in the diabetic patients of groups 1 and 2, but group 1 was also treated with captopril and diuretics like the CHF patients of group 3. Plasma zinc levels were statistically similar in all three groups, but urinary zinc excretion (mumol/24 h) and urinary zinc: creatinine (mumol/mmol) ratio were significantly higher in the type II diabetics and CHF group (27.2 +/- 1.5; 1.69 +/- 0.6, respectively) compared to the diabetic patients alone (19.4 +/- 0.76; 0.97 +/- 0.3, respectively) and the CHF patients (9.7 +/- 0.3; 0.62 +/- 0.3, respectively). and the CHF patients (9.7 +/- 0.3; 0.62 +/- 0.3, respectively). Patients with type II diabetes mellitus and CHF were treated with higher doses of captopril than the CHF patients (56.25 +/- 24 mg vs 18.8 +/- 11 mg P < 0.05). Thus, patients with type II diabetes mellitus and CHF excrete larger amounts of zinc, which may eventually lead to zinc deficiency.

[Endotracheal intubation and mechanical ventilation in severe asthma].

Retrospective analysis of all patients with acute bronchial asthma who required intubation and mechanical ventilation was performed in 1987-1993. Our study group comprised 29 patients with a total of 31 episodes of mechanical ventilation. Indications for intubation and ventilation were cardio-respiratory arrest in 9 episodes, and deterioration of clinical status despite aggressive therapy in 22 episodes. Mechanical ventilation strategy was to avoid high air-way pressures of more than 50 cm H2O even if respiratory acidosis persisted. The risk of barotrauma was thus eliminated; other complications were few and reversible, and all patients survived. We conclude that intubation and mechanical ventilation in severe asthma is beneficial and safe, and the prognosis very good.

[Central venous catheterization via the axillary vein].

Central venous catheterization is a common procedure in the intensive care unit. The vessels usually selected for access include those of the arm and the external and internal jugular, subclavian and femoral veins. We find the axillary vein also suitable. It is a safe and reliable route with few complications, and is especially recommended in ventilated and/or tracheotomized patients. We describe our experience in 80 patients, with a success rate of 90% and very few complications.

Noninvasive positive pressure ventilation in acute asthmatic attack.

Asthma is characterised by reversible airway obstruction. In most patients, control of disease activity is easily achieved. However, in a small minority, asthma may be fatal. Between the two extremes lie patients with severe asthmatic attacks, refractory to standard treatment. These patients are at an increased risk of recurrent severe attacks, with respiratory failure, and mechanical ventilation. Invasive mechanical ventilation of the asthmatic patient is associated with a higher risk of complications and, therefore, is a measure of last resort. Noninvasive positive pressure ventilation (NPPV) is another treatment modality that may be beneficial in patients with severe asthmatic attack who are at an increased risk of developing respiratory failure. These patients have the potential to benefit from early respiratory support in the form of NPPV. However, reports of NPPV in asthmatic patients are scarce, and its usage in asthmatic attacks is, therefore, still controversial. Only a few reports of NPPV in asthma have been published over the last decade. These studies mostly involve small numbers of patients and those who have problematic methodology. In this article we review the available evidence for NPPV in asthma and try to formulate our recommendations for NPPV application in asthma based on the available evidence and reports.

Critically ill obstetrical patients: outcome and predictability.

OBJECTIVE: To determine the applicability of the Acute Physiology and Chronic Health Evaluation (APACHE) II scoring system in predicting outcome in a subgroup of critically ill obstetrical patients. DESIGN: Retrospective data collection. SETTING: A multidisciplinary intensive care unit (ICU) in a university hospital. PATIENTS: All patients (n = 1,670) admitted for > 24 hrs to the ICU during an 8-yr period, of whom 58 were obstetrical patients and 120 were nonobstetrical young women. MEASUREMENTS AND MAIN RESULTS: The mean APACHE II score in the obstetrical group was 11, with a mortality risk of 16.6%. In this group, the mortality ratio, which is the ratio between actual and predicted mortality rate, was low (0.416) and significantly (p = .021) different from the expected mortality ratio of 1. The mean APACHE II score in the group of nonobstetrical young women was 10, with a mortality risk of 10.17%. In all nonobstetrical ICU patients including all the admitted patients excluding the obstetrical patients, the mean APACHE II score was 15, with a mortality risk of 24.18%. The mortality ratio in the nonobstetrical young women group and in the nonobstetrical ICU patient group was 0.986 and 1.006, respectively, which was nonsignificantly different from the expected mortality ratio. CONCLUSIONS: Obstetrical patients requiring intensive care in our ICU had a better outcome than predicted, as expressed by a low mortality ratio. Various explanations that may be applicable to any subgroup of critically ill patients with a different mortality ratio are presented. The subgroup itself may be uniquely different, similar to our obstetrical patients with their physiologic changes of pregnancy. Another explanation may relate to an improvement in care of the subgroup and therefore a better outcome.

Acute subdural hematoma following disseminated intravascular coagulation associated with an obstetric catastrophe.

The clinical, laboratory, radiological and operative recordings of a patient with disseminated intravascular coagulation (DIC) related to therapeutic abortion is reported. During a comatose state following respiratory arrest, anisocoria with right dilated unreactive pupil and decerebration signs appeared. A brain CT scan showed a right frontotemporal hemorrhage. On surgical intervention a subdural hematoma was found and removed. The patient remained in a persistent vegetative state. The rarity of subdural hematoma complicating DIC is presented and the causes of intracranial bleeding in obstetrics are reviewed.

Acute tumour lysis syndrome with extreme metabolic abnormalities.

Tumour lysis syndrome, manifested by various metabolic derangements, is a known complication after treatment of some lymphoid malignancies. A patient is reported with acute lymphocytic leukaemia who developed a tumour lysis syndrome following intensive chemotherapy. All the known complications of the syndrome were present in the most severe form--hyperuricaemia of 1.44 mmol/l, hyperphosphataemia of 7.7 mmol/l with acute oliguric renal failure and extreme hyperkalaemia of 9.8 mmol/l with electrocardiographic changes. This life-threatening condition did not respond to conservative measures and the patient recovered only after haemodialysis.

Moderate hypothermia after cardiac arrest of 17 minutes in dogs. Effect on cerebral and cardiac outcome.

Moderate hypothermia (30 degrees C) induced before circulatory arrest is known to improve neurologic outcome. We explored, for the first time in a reproducible dog outcome model, moderate hypothermia induced during reperfusion after cardiac arrest (resuscitation). In three groups of six dogs each (N = 18), normothermic ventricular fibrillation cardiac arrest (no blood flow) of 17 minutes was reversed by cardiopulmonary bypass--normothermic in control group I (37.5 degrees C) and hypothermic to 3 hours in groups II (32 degrees C) and III (28 degrees C). Defibrillation was achieved in less than or equal to 5 minutes and partial bypass was continued to 4 hours, controlled ventilation to 20 hours, and intensive care to 96 hours. All 18 dogs survived. Electroencephalographic activity returned significantly earlier in groups II and III. Mean +/- SD best neurologic deficit between 48 and 96 hours was 44 +/- 8% in group I, 38 +/- 12% in group II, and 35 +/- 7% in group III (differences not significant). Best overall performance category 2 (good outcome) between 48 and 96 hours was achieved in none of the six dogs in group I and in four of the 12 dogs in the combined hypothermic groups II and III (difference not significant). Mean +/- SD brain total histologic damage score was 130 +/- 22 in group I, 93 +/- 28 in group II (p = 0.05), and 80 +/- 26 in group III (p = 0.03). Gross myocardial damage was greater in groups II and III than in group I--numerically higher overall and significantly higher in group III for the right ventricle alone (p = 0.02). Moderate hypothermia after prolonged cardiac arrest may or may not improve cerebral outcome slightly and can worsen myocardial damage.

Systematic development of cerebral resuscitation after cardiac arrest. Three promising treatments: cardiopulmonary bypass, hypertensive hemodilution, and mild hypothermia.

Since 1970 we have investigated postischemic anoxic encephalopathy and potential treatments for cerebral resuscitation after cardiac arrest by cardiopulmonary-cerebral resuscitation (CPCR). The post-resuscitation syndrome has been studied at the levels of cell, organ, organism and community. Short-term and long-term models in rats, dogs, and monkeys have been developed, and an international multicenter randomized clinical trial mechanism was established. Clinical studies disproved the 5-min limit of reversible cardiac arrest and yielded other valuable data on treatments and prognostication. Thiopental loading or calcium entry blocker therapy (lidoflazine) gave no significant improvement in patients. Free radical scavengers are under investigation in the laboratory. We hypothesize that post-arrest perfusion failure and necrotizing cascades require etiology-specific combination treatments. Standard (control) therapy in a current dog model of cardiac arrest (no flow) of 12.5-20 min, reperfusion with cardiopulmonary bypass, and intensive care for 72-96 h has consistently resulted in survival with brain damage. After ventricular-fibrillation (VF) arrest of 17 min, moderate hypothermia (28-32 degrees C) inconsistently improved cerebral outcome. After VF arrest of 12.5 min, hypertension plus hemodilution normalized the local (multifocal) cerebral hypoperfusion post-arrest and, again, inconsistently improved cerebral outcome. Additional mild hypothermia (34-36 degrees C), however, consistently improved cerebral outcome, whether induced before or during and after arrest.