Egbert Huettemann

Late cardiac arrhythmias after blunt chest trauma.

Objective: Case reports of two patients who developed fatal cardiac arrhythmias several days after blunt chest trauma.¶Design: Case reports.¶Setting: Surgical intensive care unit of a university hospital.¶Patients: A 23-year-old man and a 9-year-old girl with blunt chest trauma and multiple further injuries following car crashes were transferred to our institution. Although ECG on admission was normal, both patients developed fatal cardiac arrhythmias after 6 and 4 days, respectively. In both patients, post-mortem analysis confirmed myocardial contusion without coronary artery lesions. Histological findings included severe interstitial oedema, haemorrhages and infiltration of lymphocytes and neutrophils, fresh myocardial necrosis and fatty degeneration.¶Conclusion: Blunt chest trauma with myocardial contusion may lead to fatal cardiac arrhythmias even after several days, particularly when other severe injuries are present. Thus, a normal ECG on admission and absence of cardiac arrhythmias during the first 24 h of intensive care treatment do not necessarily exclude the occurrence of life-threatening arrhythmias in the further course.

Anaesthesia and anti-cancer chemotherapeutic drugs.

Purpose of review This is a review of anti-cancer chemotherapeutic drugs, describing their actions, interactions, and toxicity with a particular focus on the relevance for the anaesthetist. Recent findings Anti-cancer chemotherapeutics have a vast array of adverse effects, some of which, i.e. cardiac and pulmonary toxicity, are of particular anaesthesiological relevance. Recently it has been shown that following chemotherapy with anthracyclines subtle abnormalities in cardiac function may exist even in those patients with a normal resting cardiac function, which become apparent only during anaesthesia or exercise. Children and adolescents with previous anthracycline treatment and normal cardiac function at rest had a significantly greater decrease in fractional shortening, a marker of left-ventricular systolic function, and stroke-volume index during a balanced anaesthesia with isoflurane [1 minimum alveolar concentration (MAC)] in N2O/O2. Notably, delayed cardiotoxicity (years after completed chemotherapy) has been seen only after anthracycline therapy. With respect to regional anaesthetics, one should be aware that in a considerable percentage of patients a sub-clinical, unrecognized neuropathy may be present in patients with previous chemotherapy, particularly after cisplatin treatment. Recently, a diffuse brachial plexopathy after interscalene blockade has been reported in a patient receiving cisplatin chemotherapy. Thus, if regional anaesthesia is contemplated, a detailed pre-operative neurological examination and careful assessment of the risks and benefits is warranted. Summary Anti-cancer chemotherapeutic drugs may cause generalized and specific organ toxicities and may also give rise to various unpredictable or life-threatening peri-operative complications, rendering a detailed pre-operative assessment of patients with previous chemotherapy mandatory.

Preserved Co2 Reactivity and Increase in Middle Cerebral Arterial Blood Flow Velocity During Laparoscopic Surgery in Children

In adult patients, the creation of pneumoperitoneum (PP) by means of carbon dioxide (CO2) insufflation leads to an increase in cerebral blood flow velocity (CBFV), which is thought to be caused by hypercapnia. We evaluated whether PP leads to an increase of CBFV in children, and whether this increase is directly related to PP. The effects of PP on middle cerebral artery blood flow velocity were investigated in 12 children (mean age 3 yr, range 15–63 mo) undergoing laparoscopic herniorrhaphy under general anesthesia with sevoflurane and nitrous oxide/oxygen. CBFV was measured by using transcranial Doppler ultrasonography. During CO2 insufflation, the end-tidal CO2 concentration was kept constant by adjustment of ventilation by increasing minute volume. The CBFV increased significantly at an intraabdominal pressure of 12 mm Hg compared with baseline from 68 ± 11 cm/s to 81 ± 12 cm/s (P < 0.05). CO2 reactivity remained in the normal range (4.0% ± 1.9%/mm Hg) during PP. We conclude that the induction of PP leads to an increase in middle cerebral artery blood flow velocity in young children independent from hypercapnia, whereas CO2 reactivity remains normal.

Acute left ventricular dysfunction and subarachnoid hemorrhage.

OBJECTIVE Severe left ventricular (LV) dysfunction associated with acute subarachnoid hemorrhage (SAH) due to cerebral aneurysm rupture. SETTING An adult 12-bed surgical intensive care unit of a university hospital. PATIENT A female patient presenting with SAH (Hunt & Hess grade III) and severe left ventricular dysfunction. INTERVENTIONS Central venous pressure, arterial blood pressure, extravascular lung water catheter, transesophageal echocardiography, blood gas analysis, electrocardiograms, and chest x-ray for clinical management. MEASUREMENTS AND MAIN RESULTS On admission to the district hospital, an electrocardiogram (ECG) revealed a sinus rhythm with transient ST elevations. A transesophageal echocardiography showed a left ventricular ejection fraction (LV-EF) of approximately 10%. Severe LV dysfunction required inotropic and vasopressor support to maintain mean arterial pressure above 60 mmHg, while the first measurement of an extravascular lung water catheter revealed a cardiac index of 2.0 L/min/m2 and moderate hypovolemia. Despite stepwise volume loading that increased intrathoracic blood volume--an indicator of cardiac preload--from 719 mL/m2 to 927 mL/m2, cardiac index remained poor. Enoximone lead to a marked increase of cardiac index up to 3.9 L/min/m2 and LV-EF to about 30%, but had to be stopped due to thrombopenia. Surgical clipping of an intracranial aneurysm was postponed because of the impaired cardiac function and was performed on day 18 after admission. Interestingly, neurologic outcome was not as poor as might be expected from the literature. CONCLUSION Severe left ventricular dysfunction may occur in acute SAH and may necessitate delay of aneurysm surgery.