National survey of potential heart beating solid organ donors in Sweden.

Sweden has about 135 heart beating solid organ donors per year among 9.2 million inhabitants. Earlier estimations have suggested that 250-300 of potential heart beating donors might be available in the country annually. The present study is the first nationwide survey to establish the number of potential heart-beating donors, based on all patient deaths in Swedish intensive care units (ICUs). In the present study, a potential heart-beating solid organ donor was strictly defined as "a patient in an ICU on mechanical ventilation with the diagnosis of brain death." All 85 eligible ICUs reported all patient deaths over a 3 month period of October through December 2007. The instrument consisted of 10 questions. The majority of data were entered electronically by the ICU staff into the "Swedish Intensive Care Registry." The total number of reported patient deaths was 875 with 7.4% of patients who died meeting the criteria for a potential heart-beating solid organ donor. Actually 51% of them became donors. Reasons for not becoming a donor were refusals in 31%, medical reasons in 14%, impossibility to obtain consent in 1.5%, and no suitable recipient in 3%. Furthermore, 1.5% of patients did not become donors because of preferential forensic examinations. The main conclusion of the study was that the actual number of potential heart-beating solid organ donors in Sweden seems to be less than earlier estimates. Another interesting observation is the existence of a group of artificially ventilated, brain injury patients in whom the death was diagnosed by cardiac arrest. We think that this group of patient deaths deserves further investigation in future projects.

Decision making in a life-threatening cerebral condition: a comparative study of the ethical reasoning of intensive care unit physicians and neurosurgeons.

AIM: To study the support for the arguments of neurosurgeons and intensive care unit (ICU) physicians for and against life-sustaining treatment of critically ill patients, and whether neurosurgeons are less inclined to emphasize quality-of-life aspects than ICU physicians. METHODS: A postal questionnaire was sent to a random sample of ICU physicians in Sweden (n= 298) and all neurosurgeons in Sweden (n= 112). The respondents evaluated and prioritized different arguments for and against withholding neurosurgery, withdrawing life-sustaining treatment and providing drugs which may hasten death. RESULTS: The response rate was 62.5% for neurosurgeons and 73.5% for ICU physicians. Quality-of-life aspects were stressed as an important argument by the majority of both neurosurgeons and ICU physicians (76.8% vs. 54.0%); however, significantly more neurosurgeons regarded this argument as the most important (P < 0.001). A minority in both groups, although more ICU physicians (P < 0.001), supported a patient's previously expressed wish of not ending in a persistent vegetative state as the most important argument. As the case clinically progressed, a consensus regarding the arguments for decision making evolved. CONCLUSIONS: No support was found for the hypothesis that ICU physicians care more about the quality of life of a severely ill patient. Indeed, significantly more neurosurgeons emphasized the quality-of-life aspects in this particular setting. Compared with neurosurgeons, significantly more ICU physicians considered the patient's own wishes to be important.

Antithrombin treatment in patients with traumatic brain injury: a pilot study.

This study will determine if early administration of antithrombin concentrate to patients with traumatic brain injury (TBI) can inhibit or significantly shorten the time of coagulopathy. The progress of brain injury monitored by computed tomographic scan (CT) was also assessed, as was the time needed for intensive care and outcome related to Glasgow outcome scale (GOS). Twenty-eight patients with isolated brain trauma verified with CT were included in either of two parallel groups. The Glasgow coma score (GCS) was mean 7.5, and median 7.0; signifying a moderate to severe traumatic brain injury but with a mortality of only 3.5%. The patients randomized to antithrombin treatment received a total of 100 U/kg BW during 24 hours. To measure hypercoagulability, soluble fibrin (SF), D-dimer (D-d), and thrombin-antithrombin complex (TAT) were assessed together with antithrombin (AT) and routine coagulation tests. Before treatment, SF, D-d, and TAT were markedly increased in both groups. Soluble fibrin and D-dimer (measured after treatment began) appeared to decrease faster in the AT group, and there was a statistically significant difference between the groups at 36 hours for SF and at 36 hours, 48 hours, and at Day 3 for D-d. Thrombin-antithrombin complex levels were very high in both groups but, surprisingly, showed no significant difference between the groups. The authors conclude that antithrombin concentrate administered to patients with severe TBI resulted in a marginal reduction of hypercoagulation. We could not detect any obvious influence by antithrombin on brain injury progress, on CT, or on outcome or time needed for intensive care.

Plasma cortisol is often decreased in patients treated in an intensive care unit.

OBJECTIVE: To investigate the prevalence of adrenal hypofunction, as assessed by plasma cortisol (p-cortisol) and its relationship to clinical events. DESIGN: Prospective, consecutive. SETTING: General intensive care unit in a university hospital. PATIENTS: Fifty-five patients (34 men and 21 women) were studied (surgery 40 patients, hemodialysis 5, ventilator treatment 45, sepsis 21). METHODS: Morning basal levels of p-cortisol were determined. Previous reports define adrenal insufficiency to be present if p-cortisol under stressful conditions is lower than either 400 or 500 nmol/l. The tetracosactoid test (250 microg Synacthen) was performed in 16 patients and urinary 24-h excretion of cortisol in 24 (none on corticosteroid treatment). RESULTS: Median p-cortisol was 550 nmol/l (range 20-1764). In 36% of patients p-cortisol was lower than 400 nmol/l and in 47% lower than 500 nmol/l. There was a significantly increased probability (P < 0.05) of p-cortisol being below 400 nmol/l in patients admitted due to trauma or cerebral disorder and in patients on ventilator therapy or on mannitol. Thirty minutes after tetracosactoid administration p-cortisol response was lower than 200 nmol/l in 56% of the patients. CONCLUSIONS: Several patients had low p-cortisol and attenuated responses to tetracosactoid, indicative of adrenal insufficiency. There seem to be certain risk factors for adrenal hypofunction which may justify more frequent use of physiological doses of corticosteroid in selected patients.

[A killer bacteria caused fasciitis with sepsis. Prompt handling saved the patient's life]. / Mördarbakterie orsakade fascit med sepsis. Snabb handläggning räddade patientens liv.

The article consists in a case report of a patient with rapidly progressive pain in the axillary region and deterioration in his clinical condition during the course of a skin infection, found to have pectoral muscle fascitis, and in whom progressive septic shock was accompanied by multiorgan failure. Blood culture yielded streptococci group A type 1 M1. In addition to conventional intensive care, he was treated with antibiotics, inotropic drugs, plasma exchange, and infusion of antithrombin and immunoglobulin. Surgical intervention such as fasciotomy was avoided initially and later proved unnecessary as the patient recovered well.

Plasma exchange in patients with acute renal failure in the course of multiorgan failure.

Multiorgan failure (MOF) due to intoxication, trauma or sepsis in the progressive late stages always include acute renal failure (ARF). The prognosis of these patients is poor despite adequate dialysis. This study included 27 consecutive patients (20 men and 7 women, age range 15-77 years) with a rapid progress of MOF including ARF, who were treated by plasma exchange as an attempt to reverse the progress of MOF. Twenty-three of the patients suffered from a septic shock. Oliguria or anuria was present in all, dialysis was performed in 16 of them, and mechanical respiratory aid in 17. Plasma exchange was performed 1-10 times and almost exclusively by centrifuge technique, using albumin and/or liquid stored plasma (in a few cases fresh frozen plasma) as colloidal replacement fluid. Twenty-two patients survived (81%) and 5 patients died. The reasons of death were cerebral haemorrhagia, brain abscess, myocardial sudden death, relapsing sepsis from multiple hepatic abscesses and a not drained psoas abscess. All survivors could leave hospital recovered from renal failure with few other sequelae. The plasma exchange technique is easy to perform despite low blood pressures by using a vein to vein access. Plasma exchange, therefore, may be tried to reverse late stages of multiorgan failure.

Septic shock induced by group A streptococcal infection: clinical and therapeutic aspects.

During 1988 and 1989 > 500 cases of serious group A streptococcal infections were reported in Sweden, many with a fatal outcome. We report here on 11 consecutive patients with septic preshock/shock and multiorgan failure, including acute renal failure. 10 had verified group A streptococci (GAS) serotype T1M1 infections while 1 patient was culture negative but with clinical signs of severe infection and serological evidence of GAS infection. Presenting symptoms were high fever, relative bradycardia, edema and renal failure. In all patients the condition deteriorated despite conventional treatment including volume substitution and antibiotics. Systolic blood pressure was transiently < 80 mmHg in 10 patients and 9 of them needed infusion of inotropic agents to avoid fatal circulatory shock. In 9 patients respiratory aid was instituted and 7 were dialysed. Plasma exchange was performed in 7, while the remaining 4 received transfusions with blood and plasma without plasma exchange. 10 patients improved and were discharged within 8 weeks. One woman died within 2 days after admission to the hospital. Renal function recovered in all survivors, with a follow-up serum creatinine < 80 mumol/l. The complicated clinical picture in these patients with many simultaneous therapeutic events confounds the interpretation of the effect of single actions. The favourable outcome in these severely ill patients suggests that potent inotropic agents, immunoglobulin therapy and plasma exchange might be beneficial in severe streptococcal disease when conventional treatment fails.

Coronary haemodynamic effects of surgery during enflurane-nitrous oxide anaesthesia in patients with ischaemic heart disease.

The systemic and coronary haemodynamic effects of 1.5 MAC enflurane-nitrous oxide anaesthesia and abdominal surgery were investigated in nine patients with ischaemic heart disease. Anaesthesia decreased systemic blood pressure (-56%) by a combination of cardiodepression and peripheral vasodilation. A marked fall in myocardial oxygen extraction suggested a moderate coronary vasodilation. Surgery markedly increased the circulating levels of adrenaline and noradrenaline, manifested by increases in blood pressure (+76%) and systemic vascular resistance (+83%). Pulmonary capillary wedge pressure increased by 70% without any change in cardiac or stroke volume index, suggesting that the patients were performing at the horizontal part of their left ventricular function curve. Despite the marked rise in coronary perfusion pressure and a 62% increase in myocardial oxygen demand, coronary blood flow remained unaltered. This could be due either to coronary vasoconstriction overriding the normal coronary autoregulation or to an increase in coronary back pressure opposing the diastolic aortic pressure. When coronary blood flow could not increase to meet the demand for oxygen, the myocardium had to extract more oxygen to ensure appropriate oxygenation, demonstrating interference with coronary autoregulation. Surgery markedly increased myocardial extraction of adrenaline and noradrenaline. We could not find any relationship between myocardial adrenaline extraction and heart rate response to surgery or between myocardial noradrenaline extraction and changes in coronary blood flow, calculated coronary vascular resistance, incidence of myocardial ischaemia or cardiac dysrhythmias.

Effects of enflurane on coronary haemodynamics in patients with ischaemic heart disease.

The effects of enflurane with and without nitrous oxide on coronary haemodynamics and myocardial oxygenation were investigated in 11 patients with generalised atherosclerotic disease. Enflurane decreased systemic blood pressure (-50%) mainly by systemic vasodilation (SVR -41%) and to a lesser degree by impairment of cardiac performance (CO -27%). A change from 1MAC enflurane-nitrogen-oxygen (70/30) to 1MAC enflurane-nitrous oxide-oxygen (70/30) decreased blood pressure and cardiac output further (-16% and -14%). Enflurane-nitrogen-oxygen decreased coronary blood flow (-29%) and perfusion pressure (-47%). Coronary vascular resistance fell (-20%) along with decreases in myocardial oxygen consumption and extraction (-40% and -16%). Regional coronary blood flow measurements in four of the patients revealed maldistribution of blood flow. During enflurane-nitrous oxide-oxygen, myocardial oxygen consumption and extraction decreased further (-29% and -12%) without change in coronary blood flow or resistance. Myocardial ischaemia was observed in four patients during enflurane-nitrogen. During enflurane-nitrous oxide, ischaemia disappeared in two of the previously ischaemic patients and appeared in two not previously ischaemic. The regional blood flow maldistribution was abolished with nitrous oxide. It is concluded that enflurane is a powerful coronary vasodilator and in this respect slightly less potent than isoflurane. Enflurane may induce myocardial ischaemia by redistributing coronary blood flow and/or by producing hypotension. Nitrous oxide added to enflurane depresses cardiac function and augments the coronary vasodilatory effect of enflurane to a level at which coronary blood flow becomes totally pressure dependent.

Droperidol inhibits the effects of intravenous ketamine on central hemodynamics and myocardial oxygen consumption in patients with generalized atherosclerotic disease.

A 2-mg/kg dose of ketamine was administered intravenously to 16 patients with generalized atherosclerotic disease. Eight patients were given 200 mu/kg of droperidol intravenously 10 min before ketamine administration; eight patients not given droperidol served as controls. Central hemodynamics, coronary flow (thermodilution technique) and myocardial oxygen, lactate, hypoxanthine, and catecholamine balances were studied. In control patients, ketamine increased mean blood pressure by 42%, pulmonary capillary wedge pressure by 144%, mean right atrial pressure by 60%, heart rate by 15%, and systemic vascular resistance by 40% without changes in cardiac index, stroke volume index, or left ventricular stroke work index. These data indicate that cardiac performance did not increase in parallel with the rise in afterload. However, the 50% increase in myocardial oxygen demand was associated with a 48% increase in coronary blood flow without changes in coronary vascular resistance or myocardial oxygen extraction. Augmented sympathetic activity was manifested by 397% and 164% increases in plasma levels of epinephrine and norepinephrine, respectively. The hemodynamic and cardiometabolic effects of ketamine were abolished when patients were pretreated with droperidol. The increase in plasma epinephrine levels was likewise inhibited by droperidol; significantly lower plasma norepinephrine levels also were observed. These findings suggest that droperidol inhibits the cardiovascular effects of ketamine by a centrally mediated reduction in sympathetic activity and by peripheral alpha receptor blockade.

Effects of halothane on coronary haemodynamics and myocardial metabolism in patients with ischaemic heart disease and heart failure.

Halothane was administered at an end-tidal concentration of 1% to 10 patients with stable ischaemic heart disease and clinical and haemodymanic signs of moderate heart failure. Measurements of central haemodynamic variables, coronary sinus blood flow and oxygen, lactate and hypoxanthine balances over the myocardium were done before and at steady state during halothane anaesthesia. Halothane induced marked haemodynamic changes with decreases in mean arterial pressure (-43%), mean pulmonary arteriolar occlusion pressure (-42%), systemic vascular resistance (-31%), cardiac index (-20%) stoke volume index (-31%) and left and right stroke work indices (-62% and -55%, respectively). Heart rate and pulmonary vascular resistance did not change. Coronary sinus blood flow decreased in parallel with perfusion pressure, and myocardial oxygen consumption decreased (-40%), as did myocardial oxygen extraction. Rate pressure product and triple product correlated better with changes in myocardial oxygen consumption in the present subset of patients than in healthy volunteers during halothane anaesthesia. The findings suggest that halothane, through its systemic vasodilatory effect, unloads the failing left ventricle and that this peripheral action predominates over the direct cardiodepressant action of the agent. The combined findings of unchanged coronary vascular resistance, decreased myocardial oxygen extraction and absence of increasing or pathological levels of lactate and hypoxanthine in coronary sinus blood imply a direct dilatory effect of halothane on the coronary vasculature.

Beta-blockers and thoracic epidural analgesia. Cardioprotective and synergistic effects.

Seven groups of patients with and without hypertension or with ischaemic heart disease, treated with different beta blockers were investigated to study the circulatory effects of neurolept anaesthesia alone or combined with thoracic epidural analgesia from T4 to T12/L2 during abdominal surgery. The combination of thoracic epidural analgesia and neurolept anaesthesia in hypertensive subjects treated with non-cardioselective beta blockers induced slightly lower blood pressure than measured in similar patients on cardioselective beta blockers with neurolept anaesthesia only. Patients on non-selective beta blockers with intrinsic stimulatory activity (ISA) had higher blood pressure and heart rate after neurolept anaesthesia induction than patients on cardioselective blockers. During surgery, heart rate remained at a higher level in the patients treated with ISA blockers, whereas blood pressure increased to the same level as in patients with cardioselective blockers. Cardiovascular stability was, however, best maintained in the epidural group, where myocardial energy expenditure during maximal surgical stress was comparable to that in a group of healthy subjects with the same format of anaesthesia and significantly lower than in healthy subjects with neurolept anaesthesia alone. No circulatory side effects of the combination of thoracic epidural analgesia and beta blockade were seen. In patients with ischaemic heart disease, with or without non-selective beta blockade, similar haemodynamic changes were recorded following neurolept anaesthesia. During maximal surgical stress, unmasking of alpha adrenergic activity with marked rise in blood pressure was seen in the beta-blocked patients. Despite the more accelerated haemodynamic changes in the blocked patients, a lower increase in myocardial oxygen consumption was recorded compared with the non-blocked patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial oxygen consumption and coronary haemodynamics during fentanyl-droperidol-nitrous oxide anaesthesia in patients with ischaemic heart disease.

Eight patients with stable ischaemic heart disease were investigated to determine the effects of fentanyl (15 micrograms/kg) - droperidol (150 micrograms/kg) - nitrous oxide (75%) anaesthesia, without concomitant fluid challenge, on myocardial oxygen consumption and lactate uptake, and central and coronary haemodynamics. Anaesthesia induced reductions in mean arterial pressure (--35%, P less than 0.01), systemic vascular resistance (--30%, P less than 0.01), left ventricular stroke work index (--50%, P less than 0.01) and total body oxygen consumption (--23%, P less than 0.01), with no changes in heart rate, cardiac output or mean pulmonary arteriolar occlusion pressure. Mixed venous oxygen content increased (P less than 0.05). Systemic vasodilatation, circulatory adaptation to an overall lower metabolic rate, and clinically negligible cardiodepression are the likely mechanisms behind the central haemodynamic response to this form of anaesthesia. Coronary sinus blood flow (measured by the continuous thermodilution technique) decreased (P less than 0.01) in parallel with the decrease in coronary perfusion pressure. Thus coronary vascular resistance remained unchanged. As expected from the haemodynamic findings, myocardial oxygen consumption decreased (--37%, P less than 0.01). Coronary sinus oxygen content and myocardial oxygen extraction did not change, nor was myocardial lactate uptake affected. No ST-T-segment depressions or dysrhythmias were recorded. These observations indicate that myocardial oxygenation was adequate in spite of the reduction in coronary perfusion pressure. There was poor correlation between changes in myocardial oxygen consumption and rate pressure product (R = 0.455) or triple produce (R - 0.375).