Herbert Kuhnigk

Whole-Body Multislice Computed Tomography as the First Line Diagnostic Tool in Patients With Multiple Injuries : The Focus on Time

OBJECTIVE Whole-body multislice helical computed tomography (MSCT) becomes increasingly important as a diagnostic tool in patients with multiple injuries. We describe time requirement of two different diagnostic approaches to multiple injuries one with whole-body-MSCT (MSCT Trauma-Protocol) as the sole radiologic procedure and one with conventional use of radiography, combined with abdominal ultrasound and organ focused CT (Conventional-Trauma-Protocol). METHODS Observational study with retrospective analysis of time requirements for resuscitation, diagnostic workup and transfer to definitive treatment after changing from conventional to MSCT Trauma-Protocol. Group I: data from trauma patients imaged with whole-body MSCT. Group II: data of trauma patients investigated with conventional trauma protocol before the introduction of MSCT-Trauma-Protocol. RESULTS The complete diagnostic workup in group I (n = 82) was finished after 23 minutes (17-33 minutes) [median; interquartile range (IQR)] and after 70 minutes (IQR, 56-85) in group II (n = 79). The definitive management plan based on a completed diagnostic workup was devised after 47 minutes (IQR, 37-59) in group I and after 82 minutes (IQR, 66-110) in group II. CONCLUSION A whole-body MSCT-based diagnostic approach to multiple injuries might shorten the time interval from arrival in the trauma emergency room until obtaining a final diagnosis and management plan in patients with multiple injuries and might, therefore, contribute to improvements in patient care.

Anaesthetic considerations for a 2-month-old infant with suspected complex I respiratory chain deficiency.

SIR—Respiratory chain complex I deficiency is a rare subgroup of mitochondrial myopathy with heterogeneous clinical features ranging from severe multisystem disease with neonatal death to isolated myopathy caused in the majority by mutations in nuclear DNA (1,2). Anaesthetic management for complex I deficiency in a 6-year-old child (3) and, recently, for a 2-year-old child combined with Prader–Willi syndrome (4), have been described. We present the case of a 2-month-old infant with lactic acidosis due to suspected respiratory chain disorder who underwent an uneventful general anaesthetic with remifentanil and etomidate for skeletal muscle biopsy confirming the diagnosis of a respiratory chain complex I deficiency. A 2-month-old male, weighing 4110 g, was scheduled for muscle biopsy of the quadriceps muscle to confirm the suspected diagnosis of a respiratory chain defect. After pregnancy with a history of preeclampsia, the baby was born vaginally, at 37 weeks of gestation with APGAR scores 9 ⁄ 9 ⁄ 10. Within the next few hours, the infant became tachypnoeic and developed a severe lacticacidosis (lactate 16 mmolÆl, pH 7.23, BE )15.3 mmolÆl) with hypoglycaemia 0.9 mmolÆl (17 mgÆdl). He was subsequently intubated because of respiratory distress and ventilated for 8 days. Tests for systemic infection or a metabolic disorder were negative. A muscle biopsy of the quadriceps muscle was planned to confirm the diagnosis of a respiratory chain defect suspected from the combination of elevated lactate, a lactate : pyruvate ratio of 33, lactaturia, pyruvaturia, ketonuria and argininaciduria. Preoperatively, the patient was awake, afebrile (37.1 C rectal), spontaneously breathing, with reduced muscle tone. The elcetrocardiogram (ECG) was normal and echocardiography showed a small persistent foramen ovale with a small left-right shunt, good contractility and normal systolic ejection fraction. Routine blood analysis at this time revealed: haemoglobin 8.2 g dÆl; white blood cell count 7.06 · 10Æl; platelets 500 · 10Æl sodium 136 mmolÆl potassium 4.55 mmolÆl; chloride 104 mmolÆl; lactate 4.5 mmolÆl; glucose 4.5 mmolÆl (82 mgÆdl); arterial pH 7.40; paO2 6.7 kPa (51.5 mmHg); paCO2 5.8 kPa (45.0 mmHg); HCO3 28.2 mmolÆl ; BE 3.5 mmolÆl. The coagulation parameters, liver enzymes and the serum creatinine were in the normal range. The child was fasted for 4 h and then transported to the operating room without premedication. During starvation, the i.v. infusion rate and glucose administration was 5 mlÆkgÆh and 2.1 mgÆkgÆmin, respectively. Routine monitoring included pulse oximetry, ECG, rectal temperature and noninvasive blood pressure. Induction of anaesthesia was with atropine 0.025 mgÆkg, a loading dose of remifentanil 1.9 lgÆkg infused over 45 s and etomidate 0.75 mgÆkg i.v. No neuromuscular blocking agent was administered. The patient was intubated with an uncuffed tracheal tube (3.0 mm inner diameter) and ventilated with 50% oxygen in air via a pressure-controlled ventilator prepared for MH trigger free anaesthesia with a fresh patient circuit and CO2 absorber. Anaesthesia was maintained with remifentanil 0.1–0.2 lgÆkgÆmin and boluses of 0.25 mgÆkg of etomidate. Haemodynamics were stable and heart rate and blood pressure remained in the normal range (heart rate 120–145 beatsÆmin; systolic blood pressure 70–90 mmHg). Muscle biopsy from the quadriceps was uneventful. At the end of the case, after 9 min of surgery, the infusion of remifentanil was discontinued and spontaneous ventilation started within 6 min. He was extubated and transferred to the intensive care unit. We gave him 125 mg paracetamol, rectally, at the end of surgery and there were no signs of pain or postoperative distress. The lactate level 30 min after surgery was 4.2 mmolÆl with normal glucose levels. The postoperative course was uncomplicated, despite persistently high lactate levels. He was discharged home on the fifth postoperative day. The result of the muscle biopsy was available 2 months later and confirmed a respiratory chain complex I deficiency. Three months after discharge, the infant was readmitted with symptoms of congestive heart failure and, despite medical management, died from refractory congestive heart failure at 6 months. Mitochondrial diseases cause dysfunctional aerobic metabolism including several clinical features relevant to anaesthesia. The most important symptoms are spasticity, seizure disorders, respiratory weakness, central hypoventilation, conduction abnormalities, cardiomyopathy, renal and hepatic insufficiency, diabetes mellitus, lacticacidaemia and thrombocytopaenia (5). Loeffen et al. (2) presented a group of 27 patients with isolated complex I deficiency. Clinical characteristics were divided into groups of Leigh and Leigh-like syndrome, fatal infantile lacticacidosis, neonatal cardiomyopathy with lacticacidosis, macrocephaly with progressive leukodystrophy and a residual group with unspecified mitochondrial encephalomyopathy. Avoidance of stress on the aerobic metabolism provoking lacticacidosis, optimal oxygenation in the Paediatric Anaesthesia 2003 13: 83–87