Letters to the Editor Address: Thierry Girard Department of Anaesthesia University Hospital Basel Basel 4031 Switzerland e-mail:
[email protected]
Reply to ‘Malignant hyperthermia must not be excluded due to uneventful previous anaesthesias’ doi: 10.1111/j.1399-6576.2008.01654.x Sir, We thank Drs Girard and Urwyler as well as Punj et al., for their interest in our report and their important comments. We entirely agree with their statement that malignant hyperthermia should never be excluded on the basis of uneventful previous anaesthetics. We realize that we failed to mention that the agnate half-brother and half-sister themselves refused to be tested when contacted by their father. This – and not the fact that they had previously undergone several uneventful anaesthetics – was the reason for why they did not undergo further testing. T. Brob D. Steinmann
Address: Daniel Steinmann Department of Anaesthesia and Critical Care Medicine University Medical Center Freiburg Hugstetter Strasse 55 79106 Freiburg Germany e-mail:
[email protected]
An unusual complication: intravenous administration of ethyl alcohol doi: 10.1111/j.1399-6576.2008.01661.x Sir, A 26-year-old female patient was referred to our hospital after a cesarean section and a relaparotomy on the first day of surgery. She had undergone cesarean operation under epidural anesthesia on the 40th week of pregnancy in a rural hospital. She had received 2000 cm3 of crystalloid fluid and no complication had occurred during the surgery. In post-operative period 3000 cm3/day crystalloid infusion had been planned. Respiratory depression and unconsciousness had been developed and the patient had been urgently intubated seven hours after the operation. The patient had also developed hematuria, tachycardia and hypotension at the same time, and she had undergone emergency re-operation for possible hemorrhage. No hemorrhagic focus had been found at the surgical site and
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the patient was referred to our hospital as unconsciousness had persisted. Blood pressure was 105/56 mmHg and heart rate was 94/ min on admission to our Intensive Care Unit. She was confused, intubated and GKS was 5. Cerebral CT was in normal limits. Mechanical ventilation supply was maintained. In the medical record obtained from the hospital from which patient had been operated on it was noted that in the post-operative 7th hour corresponding to the time that the patient became unconscious – 75 cm3 of 70% ethyl alcohol had been administered via intravenous (IV) route accidentally. Blood gas analysis revealed acidosis and blood ethanol level was determined as 316 mg/dl. Erythema and edema was present on the dorsal aspect of her left hand due to the IV line which had been placed in the hospital from which the patient was referred. The patient received saline solution (60 cm3/h) and dextrose 5% infusion (60 cm3/h), vitamin B complex (including thiamine), and bicarbonate replacement for acidosis. After management of acidosis, the patient regained consciousness and her general situation became better in the 24th hour of the treatment. Control blood ethanol level was found to be 10 mg/dl. Mechanical ventilation supply was terminated and the patient was extubated. During the period after extubation, blood gas analysis and general condition of the patient got better and she was transferred to the Department of Obstetrics and Gynecology on the third day. The patient was discharged from the hospital without any pathological signs and symptoms after a 2-day observation in the obstetrics clinic. Ethyl alcohol (ethanol) intoxication is usually seen after oral intake; it is readily absorbed from all parts of the gastrointestinal tract due to its hydrophilic potential. The biological effects in humans refer to practically every organ and system. In acute ethanol intoxications, CNS symptoms are the first to manifest. Together with cardiac dysrhythmias, mostly atrial fibrillation, sedative effects of ethanol intoxication, even respiratory depression may develop. Findings may be tachycardia, hypotension, mydriasis, hypo- or hyperthermia at blood concentrations over 300 mg/dl. Because of tolerance, intoxication level and blood alcohol level show weak correlation. A patient surviving after a blood alcohol level of 1500 mg/dl has previously been reported in the literature (1). Following the acute intoxication with blood concentrations over 250 mg/dl, lactic acidosis, electrolyte imbalance (hyponatremia, hypopotassemia), hypoglycemia (2), leucopenia, thrombocytopenia and coagulopathies may come across. Hemodialysis may be life saving and should be considered in patients with severe ethanol intoxication (3). Hemodialysis was not needed for our patient. Although there have been reports on experimental studies on IV ethanol intoxication (4), to our knowledge there is no human case of ethanol intoxication due to IV intake in the literature. Only, an ethanol intoxication case that had developed after IV nitroglycerin use has been reported (5). In our country, both ethyl alcohol and crystalloid solutions are marketed in bottled forms and probably this might have leaded to confusion. Although our case of ethanol intoxication was due to IV administration, the symptoms were similar to those of ethanol intoxication due to oral intake. Additionally, phlebitis, as a result of local irritation, and hematuria, which might have occurred due to high alcohol concentration (70%) and rapid IV administration were present. T. Adanir A. Rencan I. Cokboz N. Karahan
Letters to the Editor
References 1. Barceloux DG, Bond GR, Krenzelok EP et al. American academy of clinical toxicology Ad hoc committee on the treatment guidelines for methanol poisoning. American academy of clinical toxicology practice guidelines on the treatment of ethanol poisoning. J Toxicol Clin Toxicol 2002; 40: 415–46. 2. Yang CC, Yang LY, Deng JF. Hypoglycemia following ethanol ingestion in children: report of a case. J Formos Med Assoc 1995; 94: 267–70. 3. Atassi WA, Noghnogh AA, Hariman R et al. Hemodialysis as a treatment of severe ethanol poisoning. Int J Artif Organs 1999; 22: 18–20. 4. Checiu M, Sandor S. The effect of ethanol upon early development in mice and rats. IV. The effect of acute ethanol intoxication of day 4 of pregnancy upon implantation and early post implantation development in mice. Morphol Embryol (Bucur) 1982; 28: 127–33. 5. Andrien P, Lemberg L. An unusual complication of intravenous nitroglycerin. Heart Lung 1986; 15: 534.
Address: Tayfun Adanir Anaesthesiology and Reanimation Clinic Izmir Ataturk Training and Research Hospital Basin sitesi – Hatay Izmir 35370 Turkey e-mail:
[email protected]
Antons syndrome in a patient with type-2 heparin-induced thrombocytopaenia (HIT) doi: 10.1111/j.1399-6576.2008.01668.x Sir, Denial of visual loss associated with bilateral occipital lobe infarction (cortical blindness) constitutes Antons syndrome (1). Heparin-induced thrombocytopaenia (2) (HIT) (type-II) is potentially a life-threatening immune-mediated adverse drug reaction after exposure to heparin. We encountered a patient who developed cortical blindness caused by thrombosis associated with type-2 HIT. A 67-year-old male patient was admitted to cardiac intensive care unit (CITU) post-operatively after the repair of his traumatic aortic arch following a road traffic accident. He was sedated and ventilated in CITU. On second post-operative day he developed severe metabolic acidosis secondary to acute renal failure for which he was started on continuous veno-venous haemofiltration (CVVH) with unfractioned heparin as an anticoagulant. Meanwhile, the patient also developed right lower lobe pneumonia with increasing respiratory support. On day 8 the patient developed a low platelet count (minimum count o3 109/dl) with other haematological investigations being normal. HIT screen (ELISA) was positive for antiplatelet antibodies (ELISA optical density titre 3.134). Other causes for thrombocytopaenia were ruled out. Promptly unfractioned heparin and low-molecular weight heparin were stopped and prostaglandin E was started to aid anticoagulation for CVVH. Associated with HIT the patient
Fig. 1. CT brain showing bilateral occipital lobe infarctions. developed bilateral lower limb ischaemic changes and a CT scan diagnosed both superior mesenteric and inferior mesenteric artery thrombosis, which was associated with small bowel failure. The patient was started on bivalrudin (a direct thrombin inhibitor and a heparin alternative) to prevent further thrombosis and to treat already existing thrombosis. When the patient was recovering and regained full consciousness it was noted that the patient was not focussing on objects and people but he denied any visual loss. A full ophthalmology consultation revealed a normal papillary reaction and optic disc appearance with loss of both visual acuity and colour vision and a cortical blindness was diagnosed. A follow-up CT scan showed bilateral occipital lobe infarction (Fig. 1). By day 32 of CITU admission patient had improved platelet count (333 109/dl) with normalised bowel function and improved lower limb circulation. Patient was registered blind and referred for further rehabilitation. Antons syndrome is a behavioural response of bilateral occipital lobe infarction and is a rare cause of blindness. Cortical blindness as part of systemic thrombosis secondary to type-2 HIT is not reported before. Prognosis of cortical blindness (3) is poor but is dependant on causative factors. In our case prompt detection of HIT, cessation of heparin compounds and starting anticoagulant bivalrudin at appropriate time helped to provide a favourable prognosis with some morbidity. H. Krovvidi A. Bhattacharjee
References 1. Misra M, Rath S, Mohanty AB. Anton syndrome and cortical blindness due to bilateral occipital infarction. Indian J Opthalmol 1989; 37: 196. 2. Franchini M. Heparin-induced thrombocytopenia: an update. Thromb J 2005; 3: 14. 3. Argenta PA, Morgan PA. Cortical blindness and Anton syndrome in a patient with obstetric hemorrhage. Obstet Gynecol 1998; 91: 810–12.
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