Uzm. Dr.Mehmet Maşuk Demirtaş

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  • Anemi

Eğitim ve Uzmanlık
İstanbul Üniversitesi Çapa Tıp Fakültesi 
Van 100. Yıl Üniversitesi Tıp Fakültesi Çocuk Sağlığı ve Hastalıkları Anabilim Dalı

A case of metastatic spinal Ewing's sarcoma misdiagnosed as brucellosis and transverse myelitis.
Caksen H1, Odabas D, Demirtas M, Kiymaz N, Anlar O, Unal O, Ugras S.
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An 11-year-old girl was admitted with back pain for 2 months, inability to walk for 15 days, and enuresis and encopresis for 2 days. She had been hospitalized with the diagnosis of brucellosis in another hospital. At presentation, she had paraplegia, sphincter dysfunction, and bilateral sensory loss below the T6 level, and was initially diagnosed with transverse myelitis caused by brucellosis. On the third day of hospitalization, however, agglutination test for brucella was negative, but it was positive for Salmonella. Therefore, transverse myelitis was considered to be due to salmonellosis. Thoracic spine magnetic resonance imaging showed an extradural, paraspinal mass at the level of T6-T7. The mass was totally extracted, and histopathological examination revealed Ewing's sarcoma. During follow-up, no improvement in paraplegia was noted and an enlarged presacral decubital ulcer developed. Aside from supportive care, local radiotherapy was applied. Unfortunately, the patient died from probable infection 9 months after the diagnosis. We emphasize that metastatic spinal Ewing's sarcoma may mimic brucellosis and transverse myelitis in childhood
To the Editor:
Organophosphate insecticides inhibit both acetylcholinesterase and pseudo-cholinesterase activities. The inhibition of acetylcholinesterase causes accumulation of acetylcholine at synapses, and overstimulation of neurotransmission occurs as a result of this accumulation. Signs of toxicity are overactivity of the parasympathetic nervous system, nausea, vomiting, diarrhea, sweating, abdominal cramps, and copious secretions (1, 2, 3). Organophosphate poisoning (OP) is infrequently observed in either children or adults in our country, Turkey (4, 5, 6, 7). In this article, we report on a child with OP mimicking a foreign body aspiration due to an unusual presentation.
A previously healthy 14-month-old boy was admitted to our Emergency Department with vomiting, and hypersalivation for 2 hours. The mother said that a soft material (probably a piece of food) was present in his mouth before the onset of the aforementioned symptoms. While she was trying to take out the material, the child swallowed it. The personal and family histories were unremarkable. On physical examination, the temperature was 36.1°C, with a respiratory rate of 52 breaths/min, a pulse rate of 150 beats/min, and systolic arterial pressure of 70 mm Hg. The weight, height, and head circumference were within normal ranges. The general condition was moderate. He had irritability, hypersalivation, dyspnea, and tachypnea. Thorax examination revealed bilateral fine crackles. Abdominal examination was normal. On laboratory investigation urinalysis was normal. The hemoglobin was 14.3 g/dL, leukocyte count was 12,000/mm3 and thrombocyte count was 551,000/mm3. On biochemical analysis, the blood glucose level was 98 mg/dL; serum sodium 137 mEq/L; potassium 4.7 mEq/L; chloride 109 mEq/L; blood urea nitrogen 10.4 mg/dL; creatinine 0.4 mg/dL; calcium 10.7 mg/dL; phosphorus 3.8 mg/dL; uric acid 6.5 mg/dL; aspartate aminotransferase 36 U/L, and alanine aminotransferase 23 U/L. Blood gas analysis showed mild respiratory alkalosis. Prothrombin and partial thromboplastin times were normal. A chest radiograph showed mild perihilar bronchopneumonic infiltration. On admission, suspecting foreign body aspiration, the patient was referred to the Department of Pediatric Surgery and brought to the operating room for emergency bronchoscopic examination under general anesthesia. During that time frequent apnea attacks were noted. Fentanyl citrate (25 μg), succinylcholine (25 mg), and propofol (30 mg) were used for anesthesia. During bronchoscopic examination, trachea and both mainstem bronchi and esophagus were examined and found to be normal. After bronchoscopic examination (3 hours after admission to the hospital), the patient could not be aroused and bilateral severe miosis (pinpoint pupils) was detected. A single dose of naloxone (0.6 mg) was given to reverse fentanyl effects with no improvement. In addition, the deficiency of pseudo-cholinesterase was considered and a packed complete blood transfusion (15 mL/kg/dose) was administrated without improvement. Atropine sulfate (0.2 mg) and neostigmine (0.3 mg) were given, but the coma did not subside. Computed tomography (CT) scan of the brain was normal. The patient was taken to the Pediatric Intensive Care Unit and mechanical ventilation was performed.
On review of the history, the mother reported that they recently used rat poison in their home and he might have ingested it. Based on this history and the abnormal clinical findings, the patient was diagnosed with OP about 10 hours after admission to the Emergency Department. Immediately, atropine sulfate (0.1 mg/dose every 30 minutes) was initiated. After three doses of atropine sulfate, his clinical status markedly improved. A total of 24 doses of atropine were given. On the second day of admission, the neurological examination was completely normal and he was discharged from the hospital. During the second week of follow-up he was symptom-free.
Excessive secretion or hypersalivation is the main sign of OP in most series (4,6,8). In the series of Sungur and Güven, including 47 patients with OP, the most frequent signs were miosis, change in mental status, hypersalivation and fasciculations (6). Complications were observed in 35 (74.4%) patients; respiratory failure (14 patients), aspiration pneumonia (10 patients), and others (11 patients). Ten patients (21.2%) required mechanical ventilation (6). Emerson et al. reviewed 69 patients with OP and found that complications overall included respiratory failure, convulsions, and aspiration pneumonia (8). Intubation and ventilation were required in 11 patients (16%) (8). Aside from these, bronchospasm, although usually a late complication, was also noted at the beginning of treatment for OP (4). It is also well known that large doses of organophosphates may cause sustained depolarization of the motor end late, leading to muscular paralysis, and death may ensue from respiratory failure (1). Our patient had hypersalivation, change in mental status, respiratory failure, and mild bronchopneumonic infiltration, but it was not known whether or not he had miosis at admission.
Organophosphates inhibit acetylcholinesterase through the phosphorylation of the enzyme. For many OPs, the reaction is irreversible, and the signs and symptoms are prolonged over time, but more recent compounds are more readily and spontaneously dissociated. As a result of inhibition of plasma cholinesterase, increased sensitivity to drugs hydrolyzed by this enzyme can occur, e.g., succinylcholine and mivacurium (1, 3, 9). Selden and Curry reported a case of prolonged succinylcholine-induced paralysis in a child with organophosphate insecticide poisoning (10). Şener et al reported a similar case of more prolonged succinylcholine-induced paralysis in a child with undiagnosed acute organophosphates insecticide poisoning (9). They noted that a 7-hour period of apnea and paralysis after administration of succinylcholine was attributed to the decreased rate of succinylcholine metabolism resulting from inhibition of pseudocholinesterase by the insecticide. In 1997, Thompson and Stocks reported a 2-year-old boy with OP (11). In their patient, fever and somnolence developed within minutes, followed by progressive respiratory distress and stridor, without generalized weakness. The child’s condition progressed to complete airway obstruction, and intubation was necessary. Emergency laryngoscopy and bronchoscopy were performed to rule out epiglottitis or a foreign body. Instead, a bilateral vocal cord paralysis was found. The paralysis lasted 2 days before completely resolving. Insecticide poisoning was suspected. They theorized that the patient manifested a combination of the acute-type syndrome, due to the immediacy of the onset of the symptoms (i.e., fever and somnolence), and the intermediate-type syndrome, due to the transient vocal cord paralysis (11). We also suspected a foreign body aspiration in our patient, but bronchoscopic examination was found to be normal. When obtaining a detailed history, the patient was diagnosed with rat poison containing OP about 10 hours after admission to the Emergency Department. Because succinylcholine was used during anesthesia, the prolonged coma was probably due to the administration of succinylcholine. We frequently encounter OP in children who have accidentally ingested the rat poison that is produced by plants in our region. However, we could not isolate the active ingredient of the poison due to lack of laboratory facility.
In conclusion, we would like to emphasize that cases of OP may mimic a foreign body aspiration in children; therefore, a detailed history should be obtained and physical examination should carefully be performed. Otherwise, certain drugs (particularly succinylcholine) used during general anesthesia will increase the symptoms and signs and prolong the course of the ingestion.
1.    1Mayer, B.W. and Schlackman, N. Organophosphates—a pediatric hazard. Am Fam Physician. 1975; 11: 121–124
2.    2Hayes, M.M., van der Westhuizen, N.G., and Gelfand, M. Organophosphate poisoning in Rhodesia. A study of the clinical features and management of 105 patients. S Afr Med J. 1978; 54: 230–234
3.    3Landrigan, P.J. and Etzel, R.A. Chemical pollutants. in: R.E. Behrman, R.M. Kliegman, H.B. Jenson (Eds.) Textbook of pediatrics. 16th edn. WB Saunders, Philadelphia; 2000: 2152–2154
4.    4Öztürk, M.A., Keleştimur, F., Kurtoǧlu, S., Güven, K., and Arslan, D. Anticholinesterase poisoning in Turkey—clinical, laboratory and radiologic evaluation of 269 cases. Hum Exp Toxicol. 1990; 9: 273–279
5.    5Kurtoǧlu, S., Çaksen, H., and Poyrazoǧlu, M.H. Neonatal poisonings in middle Anatolia of Turkey (an analysis of 72 cases) . J Toxicol Sci. 2000; 25: 115–119
6.    6Sungur, M. and Güven, M. Intensive care management of organophosphate insecticide poisoning. Crit Care. 2001; 5: 211–215
7.    7Kara, I.H., Gülog̈lu, C., Karabulut, A., and Orak, M. Sociodemographic, clinical, and laboratory features of cases of organic phosphorus intoxication who attended the Emergency Department in the Southeast Anatolian Region of Turkey. Environ Res. 2002; 88: 82–88
8.    8Emerson, G.M., Gray, N.M., Jelinek, G.A., Mountain, D., and Mead, H.J. Organophosphate poisoning in Perth, Western Australia, 1987–1996. J Emerg Med. 1999; 17: 273–277
9.    9Şener, E.B., Üstün, E., Kocamanoǧlu, S., and Tur, A. Prolonged apnea following succinylcholine administration in undiagnosed acute organophosphate poisoning. Acta Anaesthesiol Scand. 2002; 46: 1046–1048
10.    10Selden, B.S. and Curry, S.C. Prolonged succinylcholine-induced paralysis in organophosphate insecticide poisoning. Ann Emerg Med. 1987; 16: 215–217
11.    11Thompson, J.W. and Stocks, R.M. Brief bilateral vocal cord paralysis after insecticide poisoning. A new variant of toxicity syndrome. Arch Otolaryngol Head Neck Surg. 1997; 123: 93–96
Comparison of nifedipine and captopril in children with pulmonary hypertension due to bronchopneumonia.
Uner A1, Dogan M, Demirtas M, Açikgöz M, Temel H, Kaya A, Caksen H.
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This study included 40 children, who were diagnosed with pneumonia and pulmonary hypertension (from the radiographic and clinical features), was performed at Yuzuncu Yil University Faculty of Medicine, Department of Pediatrics, from September 2003 to July 2005. Patients who had pneumonia and congenital heart disease or systemic hypertension or renal and liver disease together were excluded from the study. Blood gas analysis and oxygen concentration, measured with pulse oximetry, were performed in all patients. Besides chest X-ray, electrocardiography and echocardiographic search was also carried out. Echocardiographic examination was performed by using M mode, two-dimensional echocardiography and colored Doppler sonotron Vingmed CFM 725. At echocardiographic examination, pulmonary hypertension is defined as above 35 mmHg of pulmonary artery pressure. For echocardiographic examination, patients with pulmonary hypertension were divided into two groups. Captopril (2 mg/kg/day, three doses a day) and nifedipine (0.5 mg/kg/day, three doses a day) were given to the first and the second group, respectively. Echocardiography was performed daily until normal pulmonary artery pressure was achieved. At the beginning of the treatment, the patients were treated with double antibiotics and antibiotic change was carried out in needed cases at the follow up. Digoxin was administered to the cases of respiratory infection with heart failure.