Potassium Permanganate Poisoning-A Rare Cause of Fatal Self Poisoning

motor signs. For this reason we believe patients electrophysiological evaluation of 16 patients presenting with dyspnoea. Am Rev Respir Dis 1993;147:66-71. J Accid Emerg Med: first published as 10.1136/emj.14.1.43 on 1 January 1997. Downloaded from presenting with severe, unexplained shoulder 7 Ferrini L, Della Torre P, Preticoni G, Cantisani TA. Neural- girdle pain should be offered follow up, prefer- gic amyotrophy of the shoulder girdle; the Parsonage- Turner syndrome. Ital J Orthop Traumatol 1986;12:223- ably by their general practitioner. If motor 31. signs develop, the diagnosis can be confirmed 8 Cumming WJK, Thrush DC, Kenwood DH. Bilateral neuralgic amyotrophy complicating Weil's disease. Postgrad with EMG and the patient reassured that the Med J 1978;54:680-1. prognosis is excellent. 9 Reutens DC, Dunne JW, Leather H. Neuralgic amyotrophy following recombinant DNA hepatitis B vaccination. Mus- We thank Dr L A Loizou, Consultant Neurologist, for his help cle Nerve 1990; 13;461. in the preparation of the manuscript. 10 Malow MA, Dawson DM. Neuralgic amyotrophy in associ- ation with radiotherapy for Hodgkin's disease. Neurology 1 Parsonage NJ, Turner JWA. Neuralgic amyotrophy-the 1991;41:440-1. shoulder girdle syndrome. Lancet 1948;i:973-8. 11 Wyburn-Mason R. Brachial neuritis occurring in epidemic 2 Aymond JK, GoldnerJL, Hardaker WT. Neuralgic amyotro- form. Lancet 1941;ii:662-3. phy. Orthop Rev 1989;12:1275-9. 12 Bardos V, Somodska V. Epidemoilogic study of a brachial 3 Tonali P, Uncini A, Di Pasqua DG. So called neuralgic plexus neuritis outbreak in north east Czechoslovakia. amyotrophy: clinical features and long-term follow-up. Ital World Neurol 1961;2:973-9. J Neurol Sci 1983;4:431-7. 13 Sierra A, Prat J, Bas J, Romeu A, Montero J, Matos JAM, et 4 Rifisch A, van Laack W Neuralgic amyotrophy of the lum- al. Blood lymphocytes are sensitised to brachial plexus bar area. Arch Orthop Trauma Surg 1989;108:329-32. nerves in patients with neuralgic amyotrophy. Acta Neurol 5 Pierre PA, Laterre CE, van den Bergh PY. Neuralgic amyo- Scand 1991;82:183-6. trophy with involvement of cranial nerves IX, X, XI and 14 Devathasan G, Tong HI. Neuralgic amyotrophy: criteria for XII. Muscle Nerve 1990; 13:704-7. diagnosis and a clinical with electromyographical study of 6 Mulvey DA, Aquilina RJ, Elliot MW, Moxham J, Green M. 21 cases. Aust NZ J Med 1980; 10: 188-91. Diaphragmatic dysfunction in neuralgic amyotrophy: an

CASE REPORTS

Potassium permanganate poisoning-a rare cause of fatal self poisoning

K L Ong, T H Tan, W L Cheung http://emj.bmj.com/

Abstract Although the chemical is readily available, Attempted suicide by self poisoning is potassium permanganate poisoning is not common because of the ready availability common. of drugs, whether prescribed or bought over the counter. In some cases, the inges-

Case report on September 25, 2021 by guest. Protected copyright. don of seemingly innocuous household Our patient was a 24 year Chinese female with products or chemicals can result in death. no previous psychiatric history. She ingested an Potassium permanganate is an example. unknown quantity of potassium permanganate Poisoning with potassium permanganate crystals after a domestic quarrel. She was Department of can be fatal when a significant amount is immediately stopped by her relative and then Accident and ingested, as shown by a patient who drank a large amount of water. No other drug Emergency, Prince of suffered both the corrosive and systemic was ingested. was Wales Hospital, Shatin, She first seen at a district Hong Kong toxic effects ofthis chemical. hospital where gastric lavage was performed K L Ong (JAccid Emerg Med 1997;14:43-45) before her transfer to our department. W L Cheung Keywords: potassium permanganate poisoning; liver On arrival, she was alert and oriented. Her damage; kidney damage; laryngeal oedema airway was patent and she had no stridor. Department of There were brownish black stains on her hands Diagnostic Radiology, and Caritas Medical lips. There were similar staining of the Centre, Kowloon, entire oropharynx. The tongue and lips were Hong Kong Potassium permanganate is a readily available swollen and bled on contact. Direct laryngos- T H Tan over the counter agent that is widely used as an copy under local anaesthesia showed a stained antiseptic for baths in patients with eczema- and oedematous pharynx, with gross swelling Correspondence to: particularly the exudative types-due to its of the laryngeal structures. She was anaesthe- Dr Ong Kim Lian, Department of Accident and astringent properties. Historically its uses have tised, intubated, and ventilated and was admit- Emergency, Prince of Wales been interesting: it has been used as an aborti- ted to the intensive care unit. Hospital, Shatin, New facient,' as a urethral irrigation fluid for Initial chest x ray was normal. Oesophago- Territories, Hong Kong. treatment of gonorrhea, as a fluid for stomach scopy soon after admission showed staining of Accepted for publication washout in cases of alkaloid poisoning, and in the upper oesophagus. The rest ofthe oesopha- 12 July 1996 the solid form as a local remedy for snake bite.2 gus, stomach, and duodenum were normal, 44 Ong, Tan, Cheung

with no evidence of burn or perforation. laryngeal oedema and this would probably Follow up oesophagoscopy two days after have progressed to upper airway obstruction J Accid Emerg Med: first published as 10.1136/emj.14.1.43 on 1 January 1997. Downloaded from admission was normal. with time. Activated charcoal and broad spectrum anti- Manifestations of the gastrointestinal effects biotics were given after admission. Renal and include nausea and vomiting in the mild cases. liver function tests and complete blood picture Burns and ulceration of the mouth, oesopha- were done and all were normal. Toxicological gus, and stomach occur and are due to its screen for paracetamol was negative. Serum caustic action. It combines with proteins to amylase was normal. Methaemoglobinaemia form proteinates and with fats to form soaps, level was normal at 0.5%. resulting in necrotic ulcers which may continue During the first 24 hours after admission, to penetrate for days7 and may lead to perfora- her vital signs were stable although she tion. Early oesophagoscopy is recommended to required up to six litres of colloid to maintain assess the severity of the oesophageal burns, her pulmonary artery wedge pressure. At about although the manganese staining may obscure 36 hours she deteriorated with cardiovascular the area of the burn. Haemorrhagic pancreati- instability despite fluid loading and required tis has also been reported in a patient who adrenaline infusion. She developed dissemi- ingested 20 g of potassium permanganate8 but nated intravascular coagulation with falling this was not seen in our patient. Late platelet count and prolonged activated partial complications of upper gastrointestinal ulcera- thromboplastin time. Her liver function started tion include oesophageal stricture9 and pyloric to deteriorate, with rising alanine aminotrans- stenosis.10 Hepatic and renal damage has been ferase. By 48 hours she showed a clinical well documented and in one patient, liver picture of acute hepatic necrosis which later damage occurred after self injection of potas- deteriorated into fulminant hepatic failure. She sium permanganate into the chest." Our was oliguric with a rising creatinine level due to unfortunate patient suffered both the hepatic acute tubular necrosis, and by 72 hours she and renal toxic effects of potassium permanga- required continuous veno-venous haemofiltra- nate. tion due to renal failure. By now she showed Methaemoglobinaemia has been reported,12 signs of adult respiratory distress syndrome. although it did not occur in our patient. There was progressive cardiovascular failure Cardiovascular depression and collapse with and on day 6 she went into asystole and could shock is another feature of severe potassium not be resuscitated. permanganate poisoning although the patho- Necropsy examination showed severe fatty genesis is uncertain and it is often the cause of change and necrosis of the liver, consolidation death in those who do not succumb to the of the lungs, and petechial haemorrhages of the immediate threat of airway obstruction or mas- subcortical and papillae regions of the kidneys, sive haemorrhage due to gastrointestinal ero- and these were consistent with her clinical sions. findings. Serum manganese concentrations on The mainstay in the treatment of potassium

day 5 and day 6 were between 756 and 1629 permanganate is supportive. The immediate http://emj.bmj.com/ ptmol/litre (a level above 100 [tmol/litre is priority is to secure the airway. Although toxic). gastric lavage has been recommended by some,6 it is potentially hazardous7 as there is danger of perforation. The effectiveness of Discussion activated charcoal is not known in potassium Potassium permanganate is a powerful oxidis- permanganate poisoning and thus its adminis- ing agent and it reacts with tissue to produce a tration is controversial. of milk or Drinking on September 25, 2021 by guest. Protected copyright. coagulation type of necrosis similar to that pro- water may have a diluting and neutralising duced by acid. It is readily reduced by organic effect.13 Early oesophagoscopy is useful to matter and sometimes milk and egg white have determine the extent of upper gastrointestinal been given to reduce toxicity. injury. Useful investigations include liver and The probable lethal adult dose of potassium renal function tests, methaemoglobin level, permanganate is 10 g4 or the equivalent of 1.5 serum amylase, and serum manganese. Other teaspoons of crystals.3 supportive treatment includes the administra- Potassium permanganate is absorbed poorly tion of methylene blue and vitamin C for by the gastrointestinal tract but systemic symp- methaemoglobinaemia12 and broad spectrum toms may result from oral exposure.5 Our antibiotics in view of the risk ofperforation and patient appeared to have absorbed most of the subsequent peritonitis. The use of corticoster- potassium permanganate from the oropharyn- oids is controversial although it has been geal region as there was little evidence of the postulated that they minimised tissue oedema chemical in the rest of the gastrointestinal and the pathological inflammatory response in tract, judging by the absence of staining or cor- one patient.13 rosive effect in the lower oesophagus and the Thus what appears to be a harmless topical stomach and yet a markedly raised serum agent can, when ingested in sufficient amounts, manganese level. result in widespread systemic toxicity that can The immediate concern after the ingestion cause much morbidity and even mortality. of potassium permanganate is the threat of 1McDonough JF. Vaginal bleeding from potassium perman- acute laryngeal oedema6 and this necessitates ganate as abortifacient. N Engl J Med 1945;232:189. early endotracheal intubation or even emer- 2 Willimott SG, Freiman M. Potassium permanganate poisoning. BMJ 1936;i:58-9. gency surgical airway. Although this patient did 3 Cowie RL, Escreet BC. Potassium permanganate toxicity. not have stridor at presentation, there was South Aft Med J 1981;60:304. Inadvertent intracranial insertion ofan NG tube 45

4 Deichmann WB, Gerarde HW. Toxicology of drugs and 9 Kochhar R, Das K, Mehta SK. Potassium permanganate chemicals. New York: Academic Press, 1969. induced oesophageal stricture. Hum Toxicol 1986;5:393-4. J Accid Emerg Med: first published as 10.1136/emj.14.1.43 on 1 January 1997. Downloaded from 5 Ellenhorn MJ, Barreloux DG. Metals and related com- 10 Dagli AJ, Golden D, Finkel M, Austin E. Pyloric stenosis pounds. In: Medical toxicology-diagnosis and treatment following ingestion of potassium permanganate. Am J Dig of human poisoning. New York, Elsevier, 1988:1057-8. Dis 1973;18:1091-4. 6 Gosselin RE, Smith RP, Hodge HC. Clinical toxicology of 11 Lustig S, Pitlik SD, Rosenfeld JB. Liver damage in acute commercial products. Baltimore: Williams & Wilkins, self-induced hypermanganemia. Arch Intern Med 1982; 1984. 142:405-6. 7 Dreisbach RH, Robertson WO. Handbook of poisoning: 12 Mahomedy MC, Mahomedy YH, Canham PA, Downing prevention, diagnosis and treatment. California: Lange JW, Jeal DE. Methaemoglobinaemia following treatment Medical Publications, 1983. dispensed by witch doctors. Two cases of potassium 8 Middleton SJ, Jacyna M, McClaren D, Robinson R, permanganate poisoning. Anaesthesia 1975;30:190-3. Thomas HC. Haemorrhagic pancreatitis-a cause of death 13 Southwood T, Lamb CM, Freeman J. Ingestion of in severe potassium permanganate poisoning. Postgrad potassium permanganate crystals by a three year old boy. Med 1990;66:657-8. MedJ Aust 1987;146:639-40.

Inadvertent intracranial insertion of a nasogastric tube in a non-trauma patient

R M Freij, S T H Mullett

Abstract oxygen, an oropharyngeal airway was inserted, Complications following nasogastric intu- and intravenous fluids were given. The history bation in patients with basal skull frac- obtained from her husband was of several tures are well documented. This report is hours vomiting before the fit, but no history of of a rare cause of inadvertent intracranial any febrile illness or upper respiratory tract placement of a nasogastric (NG) tube in a symptoms. She had been epileptic for' 12 years, non-trauma patient. The patient subse- and despite taking vigabatrin (Sabril) and quently died. The use of NG tubes, their sodium valproate was poorly controlled. Of place in airway management, and lessons relevance in her past medical history was that she to be learned from this case are discussed. had suffered from an episode of pneumococcal (7Accid Emerg Med 1997;14:45-47) meningitis before the start ofher epilepsy. On examination she was pyrexial (38.4°C) Keywords: nasogastric tube; aspiration; airway; fronto- with a tachycardia of 130 beats/min. There was ethmoidal defect decreased air entry to the right lung base, con- Case report sistent with aspiration, later confirmed by chest A 59 year female patient with a history of radiograph. Her Glasgow coma score was http://emj.bmj.com/ known epilepsy presented to our accident and between 6 and 10. Further examination emergency (A&E) department in status epilep- revealed no other abnormalities. ticus of six hours' duration. The fit was termi- She was nursed in the recovery position. To nated on arrival by administering intravenous reduce the risk of further aspiration the diazepam. She was resuscitated with high flow insertion of a nasogastric tube (NG) was

Department of ------Accident and __- ._ i~~~~~~~~~~~~~~~~~. Emergency Medicine, Central Middlesex ~~~~~~III~~~~~~~~~~~~. Hospital, Acton Lane, Park Royal, London NWIO 7NS R M Freij S T H Mullett

Correspondence to: R M Freij FRCS, Registrar in Accident and Emergency Medicine. e-mail 101453.2323@' compuserve.com Accepted for publication 17 July 1996 Figure 1 Computerised tomography scan showing the intracranial placement ofthe nasogastric tube.