Inadvertent intracranial insertion of an NG tube 45

4 Deichmann WB, Gerarde HW. Toxicology of drugs andchemicals. New York: Academic Press, 1969.

5 Ellenhorn MJ, Barreloux DG. Metals and related com-pounds. In: Medical toxicology-diagnosis and treatmentof human poisoning. New York, Elsevier, 1988:1057-8.

6 Gosselin RE, Smith RP, Hodge HC. Clinical toxicology ofcommercial products. Baltimore: Williams & Wilkins,1984.

7 Dreisbach RH, Robertson WO. Handbook of poisoning:prevention, diagnosis and treatment. California: LangeMedical Publications, 1983.

8 Middleton SJ, Jacyna M, McClaren D, Robinson R,Thomas HC. Haemorrhagic pancreatitis-a cause of deathin severe potassium permanganate poisoning. PostgradMed 1990;66:657-8.

9 Kochhar R, Das K, Mehta SK. Potassium permanganateinduced oesophageal stricture. Hum Toxicol 1986;5:393-4.

10 Dagli AJ, Golden D, Finkel M, Austin E. Pyloric stenosisfollowing ingestion of potassium permanganate. Am J DigDis 1973;18:1091-4.

11 Lustig S, Pitlik SD, Rosenfeld JB. Liver damage in acuteself-induced hypermanganemia. Arch Intern Med 1982;142:405-6.

12 Mahomedy MC, Mahomedy YH, Canham PA, DowningJW, Jeal DE. Methaemoglobinaemia following treatmentdispensed by witch doctors. Two cases of potassiumpermanganate poisoning. Anaesthesia 1975;30:190-3.

13 Southwood T, Lamb CM, Freeman J. Ingestion ofpotassium permanganate crystals by a three year old boy.MedJ Aust 1987;146:639-40.

Inadvertent intracranial insertion of a nasogastrictube in a non-trauma patient

RM Freij, S T H Mullett

AbstractComplications following nasogastric intu-bation in patients with basal skull frac-tures are well documented. This report isof a rare cause of inadvertent intracranialplacement of a nasogastric (NG) tube in anon-trauma patient. The patient subse-quently died. The use of NG tubes, theirplace in airway management, and lessonsto be learned from this case are discussed.(7Accid Emerg Med 1997;14:45-47)

Keywords: nasogastric tube; aspiration; airway; fronto-ethmoidal defect

Case reportA 59 year female patient with a history ofknown epilepsy presented to our accident andemergency (A&E) department in status epilep-ticus of six hours' duration. The fit was termi-nated on arrival by administering intravenousdiazepam. She was resuscitated with high flow

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_A _

- .__ _ i~~~~~~~~~~~~~~~~~.~~~~~~III~~~~~~~~~~~~.Department ofAccident andEmergency Medicine,Central MiddlesexHospital, Acton Lane,Park Royal, LondonNWIO 7NSRM FreijS T H Mullett

Correspondence to:R M Freij FRCS, Registrarin Accident and EmergencyMedicine. e-mail101453.2323@'compuserve.com

Accepted for publication17 July 1996

oxygen, an oropharyngeal airway was inserted,and intravenous fluids were given. The historyobtained from her husband was of severalhours vomiting before the fit, but no history ofany febrile illness or upper respiratory tractsymptoms. She had been epileptic for' 12 years,and despite taking vigabatrin (Sabril) andsodium valproate was poorly controlled. Ofrelevance in her past medical history was that shehad suffered from an episode of pneumococcalmeningitis before the start of her epilepsy.On examination she was pyrexial (38.4°C)

with a tachycardia of 130 beats/min. There wasdecreased air entry to the right lung base, con-sistent with aspiration, later confirmed by chestradiograph. Her Glasgow coma score wasbetween 6 and 10. Further examinationrevealed no other abnormalities.She was nursed in the recovery position. To

reduce the risk of further aspiration theinsertion of a nasogastric tube (NG) was

Figure 1 Computerised tomography scan showing the intracranial placement of the nasogastric tube.

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Freij, Mullett

Figure 2 Plain skull radiographs; the nasogastric tube isclearly visible.

proposed. This was performed in accordancewith recognised practice.' Three attempts atinsertion were made, each of them producingblood stained fluid. When the fluid wasaspirated and tested using litmus paper therewas no colour change. The tube was left inposition after the third insertion as the fluidwas assumed to be blood stained nasalsecretions resulting from traumatic intubation.Although the resuscitation was successful in

terminating the fit, the patient remained deeplyunconscious. In view of this, and the pasthistory of meningitis, computerised tomogra-phy was undertaken. It was reported asshowing an intraventricular shunt (fig 1, A andB). Her husband, however, had no recollectionof any previous neurosurgery. Subsequentplain radiographs of the skull showed that theNG tube had passed through the skull base andwas located intracranially (fig 2, A and B). Thepatient was transferred to a neurosurgical unitwhere the NG tube was removed under radio-logical control. The patient subsequently diedfrom overwhelming sepsis.The necropsy report concluded that the

causes of death were bronchopneumonia andmeningitis. On careful examination of the skullbase, a smooth rimmed defect was noted in thefronto-ethmoidal region. This communicatedwith the roof of the nasal cavity, just lateral tothe cribriform plate, and measured 8 x 5 mm.A perforation in the dura at that point wasnoted. The pathologist suggested that thedefect may have represented a congenitalanomaly called a nasal "glioma", similar to ananterior encephalocele. Alternatively it mayhave occurred as a result of previous headtrauma.

DiscussionThe rather erroneously named nasal gliomasare rare, benign, and thought to represent het-erotopic brain tissue displaced during fetaldevelopment.2 They usually present as intra-

nasal masses in infants and children, and arecommoner in South East Asia, our patientoriginating from that area (Branfoot AC,personal communication). However, they mayoccasionally persist as a small intracranialdefect, visible only on magnetic resonanceimaging.3We are aware of only one case report of

inadvertent intracranial placement of an NGtube in an adult non-trauma patient.4 Thatcase differed from ours, in that the patient sur-vived, and it was only postulated that thecribriform plate had been thinned by a recentepisode of sinusitis, precipitating the complica-tion. There is a case report of intracranialplacement of an NG tube in an infant withoutassociated trauma.5The advanced trauma life support course6

recommends that NG tubes should not beinserted where there is the possibility of a basalskull fracture, and this is borne out by anumber of case reports.78The use of NG tubes is under scrutiny in

general. They may be a risk factor inaspiration, leading to anaerobic lung infec-tions,9 and their use after gastrointestinalsurgery has been questioned by some investiga-tors.'10 11

CONCLUSIONAlthough this case highlights an extremely rarecomplication ofNG tube insertion, certain les-sons can be learned. NG tubes havetraditionally been used to reduce the risk ofaspiration in patients with altered level of con-sciousness. However, they carry risks-as thiscase illustrates-and should never be used as asubstitute for a cuffed endotracheal tube,which remains the optimum choice for preven-tion of aspiration. We also feel that previoushead trauma or a history of adult onset epilepsyin association with meningitis should alert theclinician to the possibility of a cranial defect.NG tubes should only be used with extreme

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Traumatic asphyxia in children 47

care under these circumstances. The use of aprecurved Silastic nasopharyngeal airway tofacilitate insertion of the NG tube, as describedby Bouzarth,"2 may help prevent intracranialcomplications of this procedure.

1 Dyer I, Ashton WB. How to pass a nasogastric tube. Br JHosp Med 1991;45:45-6.

2 Azumi N, Matsuno T, Tateyama M, Inoue K. So callednasal glioma. Acta Pathol Jpn 1994;34:215-20.

3 Braun M, Boman F, Hascoet JM. Brain tissue heterotropiain the nasopharynx. Contribution ofMRI to assessment ofextension. J Neuroradiol 1992;19:68-74.

4 Glasser SA,Garfinkle W, Scanlon M. Intracranial complica-tion during insertion of a nasogastric tube. Am J Neurora-diol 1990; 11:1170.

5 van den Anker JN, Baerts W, Quak JME, Robben SGF,

Meradji N. Iatrogenic perforation of the lamina cribrosa bynasogastric tube in an infant. Pediatr Radiol 1992;22:545-6.

6 Committee on Trauma American College of Surgeons.Advanced Trauma Life Support. Core course, 1993.

7 Sacks AD. Intracranial placement of a nasogastric tube aftercomplex craniofacial trauma. Ear Nose Throat J 1993;72:800-2.

8 Katz MI, Faibel M. Inadvertent intracranial 'placement of anasogastric tube ?. Am J Roentgenol 1994; 163:222.

9 Vincent MT, Goldman BS. Anaerobic lung infections. AmFam Physician 1994;49:1815-20.

10 Schwartz CI, Heyman AS, Rao AC. Prophylactic nasogas-tric tube decompression: is its use justified? South Med J1995;88:825-30.

11 Cheatham ML, Chapman WC, Key SP, Sawyer SJL. Ameta-analysis of selective versus routine nasogastricdecompression after elective laparotomy. Ann Surg 1995;221:469-76.

12 Bouzarth W Intracranial nasogastric tube insertion. JTrauma 1978;18:818-9.

Traumatic asphyxia in children

Gregor Campbell-Hewson, Conor V Egleston, Andrew R Cope

AbstractTwo cases of traumatic asphyxia in youngchildren are reported. The first was a 2year old child run over at low speed by thefront wheels ofa delivery van. He made anuncomplicated recovery. The second childwas pinned to the floor by an empty chestof drawers in an unwitnessed accident. Hewas discovered in cardiac arrest andresuscitation was unsuccessful. The out-come foilowing traumatic asphyxia is aproduct of duration of compression andthe weight involved. Considerable weightcan be tolerated for a short period,whereas a comparatively modest weightapplied for a longer period may result indeath.( Accid Emerg Med 1997;14:47-49)

Keywords; children; crush asphyxia; traumatic asphyxia

The syndrome of traumatic asphyxia has beenreported regularly in medical publicationssince its initial description by D'AngersOllivier following his observations on thecadavers of people trampled upon duringcrowd disturbances in Paris on Bastille day1837.1 It has been defined as cervico-facialcyanosis, subconjunctival haemorrhage, andcutaneous petechial haemorrhages followingthoraco-abdominal compression.2

It was recently brought to prominence by theHillsborough Stadium disaster where thevictims bore some of the stigmata of traumaticasphyxia, although there were marked differ-ences in presentation and outcome.34The purpose of this paper is to report two

cases of traumatic asphyxia in young childrenwhich show important and contrasting featuresof the pathophysiology of this condition, and toreview the relevant published reports.

Accident andEmergencyDepartment,Addenbrooke'sHospital, CambridgeG Campbell-HewsonC V Egleston

Accident andEmergency,Peterborough DistrictHospital,PeterboroughA R Cope

Correspondence to:Dr GregorCampbell-Hewson, Accidentand Emergency Department,Addenbrooke's Hospital,Hills Road, Cambridge CB22QQ.

Accepted for publication4 September 1996.

Case 1The patient, a healthy 2 year old boy, chased aball onto a road. He fell and his torso was runover by the front wheel of a delivery van (FordTransit, unladen weight 1533-2075 kg). Thevan had been driving slowly and stoppedbefore the back wheels had reached the child.He did not lose consciousness and remainedmotionless under the van on the instructions ofhis parents.On arrival in accident and emergency (A&E)

he was alert but jittery. His blood pressure was105/55, pulse 115, respiratory rate 18, and hewas well perfused. He complained of abdomi-nal pain which was poorly localised. His facialappearance was striking, with cervicofacialcyanosis and swelling, widespread petechiae,and bilateral subconjunctival haemorrhages(figure). There were no marks of compressionon the torso. On fundoscopy there werebilateral retinal haemorrhages and exudates.Otherwise neurological examination was nor-mal. There were no fractures or other abnor-malities on radiographs of the skull, cervicalspine, or chest. A plain abdominal radiographshowed acute gastric dilatation. He was initiallytreated with oxygen, intravenous fluids, urinarycatheterisation, and insertion of a nasogastrictube to decompress the stomach. Arterialblood gases, haematology, and biochemistryprofiles were all normal. A further chest radio-graph 18 hours after the accident was also nor-mal. An ultrasound of the abdomen failed toshow any abdominal injury. Clinically he madegood progress, although his dramatic facialappearance persisted. He was discharged 8days later, by which time his appearance hadalmost returned to normal with only theresolving subconjunctival haemorrhages re-maining. The main reason for his prolongedinpatient stay was the development of a swing-ing pyrexia on day 4 caused by an urinary tractinfection, presumably secondary to catheteri-

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