Kuniko Yoshimura

Elevated S100B level in cerebrospinal fluid could predict poor outcome of carbon monoxide poisoning

OBJECTIVE S100B is a calcium-binding protein produced by astroglia in the brain and has been used as a marker of neuronal damage after brain trauma. We investigated the utility of S100B in cerebrospinal fluid (CSF) measured during the early phase of carbon monoxide (CO) poisoning in predicting the subsequent clinical course. METHODS The study included 31 patients who were admitted to the hospital with loss of consciousness following CO poisoning. S100B levels were measured by enzyme-linked immunosorbent assay in CSF, and serum samples collected simultaneously within 24 hours and on the fourth day after CO exposure. All patients were followed for at least 3 months and divided into 3 groups based on the clinical course: persistent vegetative state (PVS), delayed encephalopathy (DE), and complete recovery with no complications (NC). RESULTS During the 3-month period, 3 patients developed PVS, 5 developed DE, and 23 were classified as NC. The mean S100B levels in the CSF within 24 hours after CO exposure were higher in the PVS group (9.25 ng/mL) than in the DE (2.03 ng/mL) and NC groups (1.86 ng/mL). However, the mean serum S100B levels were not elevated in the 3 groups (0.21, 0.59, and 0.16 ng/mL, respectively). CONCLUSION Early elevation of S100B in CSF after CO poisoning could be a suitable predictor of subsequent development of PVS.

Blockade of bradykinin B2 receptor suppresses acute pancreatitis induced by obstruction of the pancreaticobiliary duct in rats

The involvement of bradykinin (BK) B2 receptor in acute pancreatitis induced by pancreaticobiliary duct ligation was investigated in rats. The activities of amylase and lipase in the serum, the water content of the pancreas, and vacuolization of the acinar cells were significantly increased 2 h after obstruction of the duct in Sprague‐Dawley rats. Elevated serum amylase activity, increased pancreatic oedema, and damage of the pancreatic tissue were significantly less marked in plasma kininogen‐deficient, B/N‐Katholiek rats than in the normal strain, B/N‐Kitasato rats 2 h after the ligation. Obstruction of the pancreaticobiliary duct augmented the level of (1‐5)‐BK (Arg1‐Pro2‐Pro3‐Gly4‐Phe5), a stable BK metabolite, in the blood from 73.0±21.7 pg ml−1 at 0 h to 149.8±38.0 pg ml−1 at 2 h after the induction of pancreatitis in SD rats. Administration of a BK B2 receptor antagonist, FR173657 (100 mg kg−1, p.o.) or Hoe140 (100 nmol kg−1, s.c.), reduced the elevation of amylase and lipase activities in the serum and of pancreatic water content in a dose‐dependent manner. The effective attenuation of oedema formation and vacuolization by the antagonists was also confirmed light‐microscopically. In contrast, treatment with gabexate mesilate or indomethacin did not cause significant suppression of the pancreatitis. These findings suggest a possible involvement of kinin B2 receptor in the present pancreatitis model. Furthermore, they point to the potential usefulness of the B2 receptor in clinical acute pancreatitis.

Effects of inhaled monoethanolamine on bronchoconstriction

We previously reported a 65‐year‐old man who aspirated an alkaline detergent containing 3.3% w/v (weight of solute per volume of solution) monoethanolamine (MEA) into his lungs, causing asthma‐like symptoms. We presently describe the mechanism of MEA‐induced bronchoconstriction according to findings in guinea pigs. In anesthetized, artificially ventilated animals, changes in airway opening pressure (Pao) were measured as an index of bronchoconstriction. An aerosol of 3.3% MEA solution (0.1 ml kg−1) inhaled through a tracheal cannula induced significantly stronger bronchoconstriction than an aerosol of potassium hydroxide (KOH) solution (0.1 ml kg−1) at the same pH. MEA‐induced bronchoconstriction was significantly suppressed by premedication with intravenously injected atropine sulfate (3 mg kg−1), a muscarinic receptor antagonist, or diphenhydramine hydrochloride (10 mg kg−1), a histamine‐H1 receptor antagonist. MEA‐induced bronchoconstriction was not enhanced by premedication with an intravenous injection of neostigmine (0.1 mg kg−1), an acetylcholinesterase inhibitor. When bronchoconstriction was induced by MEA, histamine concentrations in bronchoalveolar lavage fluid (BALF) were not significantly greater than in BALF after KOH‐induced bronchoconstriction or in BALF after inhalation of physiologic saline. In vitro, contraction of trachea denuded of epithelium during superfusion with MEA (10 mm) was suppressed by premedication with pyrilamine maleate, a histamine‐H1 receptor antagonist, at 10 and 100 µm. Contraction of trachea denuded of epithelium during superfusion with MEA (10 mm) was suppressed by premedication with atropine sulfate at 10 and 100 µm. These results suggest that asthma‐like symptoms may result partly from agonistic MEA effects at histamine‐H1 receptors and muscarinic receptors. Copyright

Aseptic meningitis in association with glyphosate-surfactant herbicide poisoning

Introduction. The mechanisms underlying early central nervous system (CNS) signs and symptoms of glyphosate-surfactant herbicide (GlySH) poisoning are unclear. Case presentation. A 58-year-old woman ingested approximately 150 mL of GlySH containing 41% glyphosate and 15% polyoxyethyleneamine. Two days later, she was admitted in the Emergency Center in a semicomatose state. Acute respiratory distress syndrome, circulatory collapse, acute renal failure, and disseminated intravascular coagulopathy were diagnosed. Meningitis was also suspected as she demonstrated Kernigs sign and significant neck stiffness with rigidity of the extremities as well as consciousness disturbance and fever (38.4°C). Investigations of cerebrospinal fluid (CSF) revealed the presence of glyphosate (122.5 μg/mL), significant elevation of IL-6 (394 μg/mL), and pleocytosis (32 cells/μL) with monocyte dominance. All bacteriological and virological tests were later found to be negative. She recovered completely after responding to aggressive supportive care in the intensive care unit. All signs and symptoms suggesting meningitis resolved as the concentration of glyphosate in CSF decreased. She was discharged on day 39 of hospitalization. Discussion. These findings suggest that the present case involved aseptic meningitis in association with GlySH poisoning. Conclusion. CNS signs and symptoms induced by aseptic meningitis should be considered in cases of glyphosate-surfactant herbicide poisoning.

Glyphosate-surfactant herbicide products containing glyphosate potassium salt can cause fatal hyperkalemia if ingested in massive amounts

Because glyphosate-surfactant herbicide (GlySH) is the most common nonselective herbicide, medical emergencies often include ingestion of GlySH products in suicide attempts. A 69-year-old woman ingested about 500 mL of a GlySH product (Roundup Maxload 1L ® , Nissan Chemical Industries Ltd., Tokyo, Japan). Her husband found her fully conscious but vomiting several times and called for an ambulance; upon reaching the Emergency center, she suddenly lost consciousness and had no pulse. Electrocardiogram (ECG) revealed ventricular tachycardia (VT); the patient received cardiopulmonary resuscitation (CPR) with endotracheal intubation and cardioversions. On admission, the patient had no pulse and an ECG demonstrating VT. CPR continued with repeated cardioversions and intravenous administration of antiarrhythmics. VT was refractory and responses to the treatments were only temporary, with the 12-lead ECG revealing tall, tapering T waves without P waves. Laboratory tests revealed extreme hyperkalemia (10.7 mEq/L) with normal renal function (BUN: 17.9 mg/dL, Cr: 0.51 mg/dL) and metabolic acidosis (pH: 7.005, PaCO 2 : 41.6 mm Hg, BE: 20.7 mmol/L, HCO 3 : 10.1 mmol/L). Percutaneous cardiopulmonary support (PCPS) and continuous hemodialysis (CHD) were initiated and 50 g of activated charcoal was administered through a nasogastric tube. Chest x-rays showed a diffuse pulmonary infi ltrate. The patient was then diagnosed with acute respiratory distress syndrome (ARDS); mechanical ventilation with high positive end-expiratory pressure and low tidal volume was induced. After PCPS and CHD, the potassium serum concentration promptly decreased to normal levels and ECG showed a normal sinus rhythm; PCPS and CHD were terminated seven and 20 h after admission, respectively. Endoscopy revealed pharyngeal edema, as well as esophageal and gastric erosions. Both the ARDS and edema gradually improved; mechanical ventilation and intubation were terminated on Day 20. Serum glyphosate levels on admission and after 18 hours were 1625.74 and 100.44 μ g/mL, respectively. GlySH products typically contain glyphosate, a surfactant and other minor ingredients. Patients who ingest GlySH products often present with hyperkalemia. 1 – 3 However, hyperkalemia is usually associated with renal dysfunction and not severe enough to cause fatal arrhythmias or cardiac arrest. The patient presented with refractory ventricular arrhythmia caused by extreme hyperkalemia shortly after ingestion of a GlySH product. Considering the normal renal function and ECG fi ndings, the most probable cause of her hyperkalemia was an excessive intake of potassium. Commercially available GlySH products generally contain glyphosate as an isopropylamine salt or partially as an ammonium salt. The product ingested by the patient has been available in Japan since 2006 and contains 48% glyphosate potassium salt. Our laboratory determined the specifi c gravity of the GlySH product to be about 1.1. Surprisingly, the product contained about 2.6 mEq/mL of potassium, and the patient took as much as 1300 mEq of potassium. We found only one case report of extreme hyperkalemia (9.22 mEq/L), in which a 65-year-old Japanese woman ingested the same GlySH product and showed ECG readings with absent P waves and tall, tapering T waves. 4 It may be problematic that GlySH products containing much potassium can be easily purchased in retail stores throughout Japan. Physicians should be aware that GlySH products containing glyphosate potassium salt can cause fatal hyperkalemia if ingested in massive amounts.

Refractory status epilepticus, circulatory collapse after cardiac arrest, and acute respiratory distress syndrome caused by severe isolated fluvoxamine poisoning: a case report

A 30‐year‐old female ingested 21.75 g fluvoxamine in a suicide attempt. She presented with grand mal seizures and vomiting on admission to our Emergency Center, with a fluvoxamine serum concentration of 4.58 μg/mL. The patient was diagnosed with status epilepticus, which could not be fully suppressed with the maximum dosage of benzodiazepines. The patient also developed circulatory collapse after resuscitation for sudden cardiac arrest and acute respiratory distress syndrome, believed to be secondary to aspiration.